Complement System Proteins
Complement Membrane Attack Complex
Complement Inactivator Proteins
Complement C3-C5 Convertases
Complement Factor B
Complement Pathway, Alternative
Complement Pathway, Classical
Receptors, Complement 3b
Complement Factor H
Receptor, Anaphylatoxin C5a
Complement Activating Enzymes
Complement Inactivating Agents
Complement Hemolytic Activity Assay
Complement C1 Inactivator Proteins
Receptors, Complement 3d
Complement Fixation Tests
Complement Factor D
Complement Factor I
Complement C4b-Binding Protein
Complement C3b Inactivator Proteins
Complement C3-C5 Convertases, Classical Pathway
Complement C3-C5 Convertases, Alternative Pathway
Complement C1 Inhibitor Protein
Complement C3 Convertase, Alternative Pathway
Complement C5 Convertase, Classical Pathway
Molecular Sequence Data
Complement C3 Convertase, Classical Pathway
Lupus Erythematosus, Systemic
Complement C5 Convertase, Alternative Pathway
Amino Acid Sequence
Complement Pathway, Mannose-Binding Lectin
Complement C5a, des-Arginine
Genetic Complementation Test
Enzyme-Linked Immunosorbent Assay
Major Histocompatibility Complex
Disease Models, Animal
Blood Bactericidal Activity
Electrophoresis, Polyacrylamide Gel
Complement C3 Nephritic Factor
Surface Plasmon Resonance
Sequence Homology, Amino Acid
Polymerase Chain Reaction
Gene Expression Regulation
Mannose-Binding Protein-Associated Serine Proteases
Adrenal Hyperplasia, Congenital
Protein Structure, Tertiary
Sequence Homology, Nucleic Acid
Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization
Reverse Transcriptase Polymerase Chain Reaction
Polymorphism, Restriction Fragment Length
Immune Adherence Reaction
Fluorescent Antibody Technique
Genetic Predisposition to Disease
Polymorphism, Single Nucleotide
Immune Complex Diseases
Immunohistochemical analysis of arterial wall cellular infiltration in Buerger's disease (endarteritis obliterans). (1/194)PURPOSE: The diagnosis of Buerger's disease has depended on clinical symptoms and angiographic findings, whereas pathologic findings are considered to be of secondary importance. Arteries from patients with Buerger's tissue were analyzed histologically, including immunophenotyping of the infiltrating cells, to elucidate the nature of Buerger's disease as a vasculitis. METHODS: Thirty-three specimens from nine patients, in whom Buerger's disease was diagnosed on the basis of our clinical and angiographic criteria between 1980 and 1995 at Nagoya University Hospital, were studied. Immunohistochemical studies were performed on paraffin-embedded tissue with a labeled streptoavidin-biotin method. RESULTS: The general architecture of vessel walls was well preserved regardless of the stage of disease, and cell infiltration was observed mainly in the thrombus and the intima. Among infiltrating cells, CD3(+) T cells greatly outnumbered CD20(+) B cells. CD68(+) macrophages or S-100(+) dendritic cells were detected, especially in the intima during acute and subacute stages. All cases except one showed infiltration by the human leukocyte antigen-D region (HLA-DR) antigen-bearing macrophages and dendritic cells in the intima. Immunoglobulins G, A, and M (IgG, IgA, IgM) and complement factors 3d and 4c (C3d, C4c) were deposited along the internal elastic lamina. CONCLUSION: Buerger's disease is strictly an endarteritis that is introduced by T-cell mediated cellular immunity and by B-cell mediated humoral immunity associated with activation of macrophages or dendritic cells in the intima. (+info)
Complement activation and expression of membrane regulators in the middle ear mucosa in otitis media with effusion. (2/194)The aetiopathogenesis of chronic otitis media with effusion (OME) in children is not yet fully understood. OME is characterized by metaplasia of the epithelium and accumulation of sticky, glue-like effusion in the middle ear containing different mediators of inflammation, including activation fragments of the complement system. Here we examined whether the fluid phase complement activation is reflected in the middle ear mucosa and how the mucosa is protected against the cytolytic activity of complement. Mucosal biopsies from 18 middle ears of children with a history of chronic OME were taken. The biopsies were analysed by immunofluorescence microscopy after staining for complement fragments iC3b/C3c, C3d and C9, and regulators membrane cofactor protein (MCP; CD46), decay-accelerating factor (DAF; CD55) and protectin (CD59). There was a strong staining for iC3b/C3c, and a weaker one for C3d and C9 on the surface of the middle ear epithelial cells of OME patients but not in controls without OME. MCP was expressed on the hyperplastic three to four outer cell layers of the epithelium, while CD59 was expressed throughout the middle ear mucosa. The results suggest a strong ongoing complement activation and consequent inflammation in the middle ear cavity. Unrestricted complement damage of the epithelial lining is prevented by the strong expression of MCP and CD59. (+info)
C6 produced by macrophages contributes to cardiac allograft rejection. (3/194)The terminal components of complement C5b-C9 can cause significant injury to cardiac allografts. Using C6-deficient rats, we have found that the rejection of major histocompatibility (MHC) class I-incompatible PVG.R8 (RT1.A(a)B(u)) cardiac allografts by PVG.1U (RT1.A(u)B(u)) recipients is particularly dependent on C6. This model was selected to determine whether tissue injury results from C6 produced by macrophages, which are a conspicuous component of infiltrates in rejecting transplants. We demonstrated that high levels of C6 mRNA are expressed in isolated populations of macrophages. The relevance of macrophage-produced C6 to cardiac allograft injury was investigated by transplanting hearts from PVG. R8 (C6-) donors to PVG.1U (C6-) rats which had been reconstituted with bone marrow from PVG.1U (C6+) rats as the sole source of C6. Hearts grafted to hosts after C6 reconstitution by bone marrow transplantation underwent rejection characterized by deposition of IgG and complement on the vascular endothelium together with extensive intravascular aggregates of P-selectin-positive platelets. At the time of acute rejection, the cardiac allografts contained extensive perivascular and interstitial macrophage infiltrates. RT-PCR and in situ hybridization demonstrated high levels of C6 mRNA in the macrophage-laden transplants. C6 protein levels were also increased in the circulation during rejection. To determine the relative contribution to cardiac allograft rejection of the low levels of circulating C6 produced systemically by macrophages, C6 containing serum was passively transferred to PVG.1U (C6-) recipients of PVG.R8 (C6-) hearts. This reconstituted the C6 levels to about 3 to 6% of normal values, but failed to induce allograft rejection. In control PVG.1U (C6-) recipients that were reconstituted with bone marrow from PVG.1U (C6-) donors, C6 levels remained undetectable and PVG.R8 cardiac allografts were not rejected. These results indicate that C6 produced by macrophages can cause significant tissue damage. (+info)
Functional properties of complement factor H-related proteins FHR-3 and FHR-4: binding to the C3d region of C3b and differential regulation by heparin. (4/194)The human factor H-related proteins FHR-3 and FHR4 are members of a family of proteins related to the complement factor H. Here, we report that the two proteins bind to the C3d region of complement C3b. The apparent K(A) values for the interactions of FHR-3 and FHR-4 with C3b are 7.5 x 10(6) M(-1) and 2.9 x 10(6) M(-1), respectively. Binding studies performed with C3b-coated pneumococci confirmed the results obtained with the biosensor system. A C-terminal construct of factor H showed similar binding characteristics. The interaction of FHR-3, but not of FHR4, with opsonised pneumococci was inhibited by heparin. (+info)
Tracing uptake of C3dg-conjugated antigen into B cells via complement receptor type 2 (CR2, CD21). (5/194)Electron microscopy was used to study the internalization and delivery of ligands for complement receptor type 2 (CR2, CD21) to endocytic compartments of B-lymphoblastoid Raji cells. Opsonized antigen was mimicked with purified C3dg conjugated to colloidal gold. C3dg-gold bound specifically to the cell surface in a time-dependent manner, and preincubation of the cells with a monoclonal antibody blocking the CR2 ligand-binding site completely inhibited any C3dg-gold binding. Notably, the binding of C3d-gold was confined to cell surface protrusions, eg, microvilli. C3dg-gold was apparently internalized through coated pits located at the bases of microvilli and could be traced to different compartments of the endocytic pathway. The morphologic characteristics and intracellular distribution of these multivesicular or multilaminar structures were compatible with those of compartments known to harbor major histocompatibility complex (MHC) class II molecules. Immunolabeling showed that the internalized C3dg-gold colocalized with MHC class II in these structures. These data provide the first ultrastructural evidence that complement-coated antigens are endocytosed by antigen-nonspecific B cells by CR2 and are delivered to the compartments in which peptide loading for antigen presentation occurs. They support the notion that CR2 may play a role in antigen presentation by B cells regardless of B-cell receptor specificity. (Blood. 2000;95:2617-2623) (+info)
Structure at 1.44 A resolution of an N-terminally truncated form of the rat serum complement C3d fragment. (6/194)Complement component C3 plays a key role in the complement-mediated immune defence, and occupies a central position within the complement cascade system. One of its degradation products, C3dg, was purified from rat serum and crystallised in two different crystal forms as N-terminally truncated fragment. Despite the truncation and the lack of a significant portion of the N-terminus as compared to C3d, the structure of the fragment is highly similar to that of recombinant human C3d (Nagar et al., Science 280 (1998) 1277-1281). Structural details of the reactive site have been obtained, suggesting a possible mode of thioester bond formation between Cys-1010 and Gln-1013 and thioester bond cleavage in the transacylation reaction involving His-1126. The truncation at the N-terminus of C3d leads to the exposure of a surface of the molecule that favours dimerisation, so that in both crystal forms, the fragment is present as a dimer, with monomers related by a two-fold axis. (+info)
Detachment of human immunodeficiency virus type 1 from germinal centers by blocking complement receptor type 2. (7/194)After the transition from the acute to the chronic phase of human immunodeficiency virus (HIV) infection, complement mediates long-term storage of virions in germinal centers (GC) of lymphoid tissue. The contribution of particular complement receptors (CRs) to virus trapping in GC was studied on tonsillar specimens from HIV-infected individuals. CR2 (CD21) was identified as the main binding site for HIV in GC. Monoclonal antibodies (MAb) blocking the CR2-C3d interaction were shown to detach 62 to 77% of HIV type 1 from tonsillar cells of an individual in the presymptomatic stage. Although they did so at a lower efficiency, these antibodies were able to remove HIV from tonsillar cells of patients under highly active antiretroviral therapy, suggesting that the C3d-CR2 interaction remains a primary entrapment mechanism in treated patients as well. In contrast, removal of HIV was not observed with MAb blocking CR1 or CR3. Thus, targeting CR2 may facilitate new approaches toward a reduction of residual virus in GC. (+info)
Structure-guided identification of C3d residues essential for its binding to complement receptor 2 (CD21). (8/194)A vital role for complement in adaptive humoral immunity is now beyond dispute. The crucial interaction is that between B cell and follicular dendritic cell-resident complement receptor 2 (CR2, CD21) and its Ag-associated ligands iC3b and C3dg, where the latter have been deposited as a result of classical pathway activation. Despite the obvious importance of this interaction, the location of a CR2 binding site within C3d, a proteolytic limit fragment of C3dg retaining CR2 binding activity, has not been firmly established. The recently determined x-ray structure of human C3d suggested a candidate site that was remote from the site of covalent attachment to Ag and consisted of an acidic residue-lined depression, which accordingly displays a significant electronegative surface potential. These attributes were consistent with the known ionic strength dependence of the CR2-C3d interaction and with the fact that a significant electropositive surface was apparent in a modeled structure of the C3d-binding domains of CR2. Therefore, we have performed an alanine scan of all of the residues within and immediately adjacent to the acidic pocket in C3d. By testing the mutant iC3b molecules for their ability to bind CR2, we have identified two separate clusters of residues on opposite sides of the acidic pocket, specifically E37/E39 and E160/D163/I164/E166, as being important CR2-contacting residues in C3d. Within the second cluster even single mutations cause near total loss of CR2 binding activity. Consistent with the proposed oppositely charged nature of the interface, we have also found that removal of a positive charge immediately adjacent to the acidic pocket (mutant K162A) results in a 2-fold enhancement in CR2 binding activity. (+info)
There are two main types of hemolysis:
1. Intravascular hemolysis: This type occurs within the blood vessels and is caused by factors such as mechanical injury, oxidative stress, and certain infections.
2. Extravascular hemolysis: This type occurs outside the blood vessels and is caused by factors such as bone marrow disorders, splenic rupture, and certain medications.
Hemolytic anemia is a condition that occurs when there is excessive hemolysis of RBCs, leading to a decrease in the number of healthy red blood cells in the body. This can cause symptoms such as fatigue, weakness, pale skin, and shortness of breath.
Some common causes of hemolysis include:
1. Genetic disorders such as sickle cell anemia and thalassemia.
2. Autoimmune disorders such as autoimmune hemolytic anemia (AIHA).
3. Infections such as malaria, babesiosis, and toxoplasmosis.
4. Medications such as antibiotics, nonsteroidal anti-inflammatory drugs (NSAIDs), and blood thinners.
5. Bone marrow disorders such as aplastic anemia and myelofibrosis.
6. Splenic rupture or surgical removal of the spleen.
7. Mechanical injury to the blood vessels.
Diagnosis of hemolysis is based on a combination of physical examination, medical history, and laboratory tests such as complete blood count (CBC), blood smear examination, and direct Coombs test. Treatment depends on the underlying cause and may include supportive care, blood transfusions, and medications to suppress the immune system or prevent infection.
The term "systemic" refers to the fact that the disease affects multiple organ systems, including the skin, joints, kidneys, lungs, and nervous system. LES is a complex condition, and its symptoms can vary widely depending on which organs are affected. Common symptoms include fatigue, fever, joint pain, rashes, and swelling in the extremities.
There are several subtypes of LES, including:
1. Systemic lupus erythematosus (SLE): This is the most common form of the disease, and it can affect anyone, regardless of age or gender.
2. Discoid lupus erythematosus (DLE): This subtype typically affects the skin, causing a red, scaly rash that does not go away.
3. Drug-induced lupus erythematosus: This form of the disease is caused by certain medications, and it usually resolves once the medication is stopped.
4. Neonatal lupus erythematosus: This rare condition affects newborn babies of mothers with SLE, and it can cause liver and heart problems.
There is no cure for LES, but treatment options are available to manage the symptoms and prevent flares. Treatment may include nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, immunosuppressive medications, and antimalarial drugs. In severe cases, hospitalization may be necessary to monitor and treat the disease.
It is important for people with LES to work closely with their healthcare providers to manage their condition and prevent complications. With proper treatment and self-care, many people with LES can lead active and fulfilling lives.
Idiopathic membranous nephropathy (IMN) is an autoimmune disorder that causes GNM without any identifiable cause. Secondary membranous nephropathy, on the other hand, is caused by systemic diseases such as lupus or cancer.
The symptoms of GNM can vary depending on the severity of the disease and may include blood in the urine, proteinuria, edema, high blood pressure, and decreased kidney function. The diagnosis of GNM is based on a combination of clinical findings, laboratory tests, and renal biopsy.
Treatment for GNM is aimed at slowing the progression of the disease and managing symptoms. Medications such as corticosteroids, immunosuppressive drugs, and blood pressure-lowering drugs may be used to treat GNM. In some cases, kidney transplantation may be necessary.
The prognosis for GNM varies depending on the severity of the disease and the underlying cause. In general, the prognosis for IMN is better than for secondary membranous nephropathy. With proper treatment, some patients with GNM can experience a slowing or stabilization of the disease, while others may progress to end-stage renal disease (ESRD).
The cause of GNM is not fully understood, but it is believed to be an autoimmune disorder that leads to inflammation and damage to the glomerular membrane. Genetic factors and environmental triggers may also play a role in the development of GNM.
There are several risk factors for developing GNM, including family history, age (GMN is more common in adults), and certain medical conditions such as hypertension and diabetes.
The main complications of GNM include:
1. ESRD: Progression to ESRD is a common outcome of untreated GNM.
2. High blood pressure: GNM can lead to high blood pressure, which can further damage the kidneys.
3. Infections: GNM increases the risk of infections due to impaired immune function.
4. Kidney failure: GNM can cause chronic kidney failure, leading to the need for dialysis or a kidney transplant.
5. Cardiovascular disease: GNM is associated with an increased risk of cardiovascular disease, including heart attack and stroke.
6. Malnutrition: GNM can lead to malnutrition due to decreased appetite, nausea, and vomiting.
7. Bone disease: GNM can cause bone disease, including osteoporosis and bone pain.
8. Anemia: GNM can cause anemia, which can lead to fatigue, weakness, and shortness of breath.
9. Increased risk of infections: GNM increases the risk of infections due to impaired immune function.
10. Decreased quality of life: GNM can significantly decrease a person's quality of life, leading to decreased mobility, pain, and discomfort.
It is important for individuals with GNM to receive early diagnosis and appropriate treatment to prevent or delay the progression of these complications.
The symptoms of glomerulonephritis can vary depending on the underlying cause of the disease, but may include:
* Blood in the urine (hematuria)
* Proteinuria (excess protein in the urine)
* Reduced kidney function
* Swelling in the legs and ankles (edema)
* High blood pressure
Glomerulonephritis can be caused by a variety of factors, including:
* Infections such as staphylococcal or streptococcal infections
* Autoimmune disorders such as lupus or rheumatoid arthritis
* Allergic reactions to certain medications
* Genetic defects
* Certain diseases such as diabetes, high blood pressure, and sickle cell anemia
The diagnosis of glomerulonephritis typically involves a physical examination, medical history, and laboratory tests such as urinalysis, blood tests, and kidney biopsy.
Treatment for glomerulonephritis depends on the underlying cause of the disease and may include:
* Antibiotics to treat infections
* Medications to reduce inflammation and swelling
* Diuretics to reduce fluid buildup in the body
* Immunosuppressive medications to suppress the immune system in cases of autoimmune disorders
* Dialysis in severe cases
The prognosis for glomerulonephritis depends on the underlying cause of the disease and the severity of the inflammation. In some cases, the disease may progress to end-stage renal disease, which requires dialysis or a kidney transplant. With proper treatment, however, many people with glomerulonephritis can experience a good outcome and maintain their kidney function over time.
Arteriolosclerosis is often associated with conditions such as hypertension, diabetes, and atherosclerosis, which is the buildup of plaque in the arteries. It can also be caused by other factors such as smoking, high cholesterol levels, and inflammation.
The symptoms of arteriolosclerosis can vary depending on the location and severity of the condition, but may include:
* Decreased blood flow to organs or tissues
* Shortness of breath
* Dizziness or lightheadedness
* Pain in the affected limbs or organs
Arteriolosclerosis is typically diagnosed through a combination of physical examination, medical history, and diagnostic tests such as ultrasound, angiography, or blood tests. Treatment for the condition may include lifestyle changes such as exercise and dietary modifications, medications to control risk factors such as hypertension and high cholesterol, and in some cases, surgical intervention to open or bypass blocked arterioles.
In summary, arteriolosclerosis is a condition where the arterioles become narrowed or obstructed, leading to decreased blood flow to organs and tissues and potentially causing a range of health problems. It is often associated with other conditions such as hypertension and atherosclerosis, and can be diagnosed through a combination of physical examination, medical history, and diagnostic tests. Treatment may include lifestyle changes and medications to control risk factors, as well as surgical intervention in some cases.
1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.
2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.
3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.
4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.
5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.
6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.
7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.
8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.
9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.
10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.
There are several types of lupus nephritis, each with its own unique characteristics and symptoms. The most common forms include:
* Class I (mesangial proliferative glomerulonephritis): This type is characterized by the growth of abnormal cells in the glomeruli (blood-filtering units of the kidneys).
* Class II (active lupus nephritis): This type is characterized by widespread inflammation and damage to the kidneys, with or without the presence of antibodies.
* Class III (focal lupus nephritis): This type is characterized by localized inflammation in certain areas of the kidneys.
* Class IV (lupus nephritis with crescentic glomerulonephritis): This type is characterized by widespread inflammation and damage to the kidneys, with crescent-shaped tissue growth in the glomeruli.
* Class V (lupus nephritis with sclerotic changes): This type is characterized by hardening and shrinkage of the glomeruli due to scarring.
Lupus Nephritis can cause a range of symptoms, including:
* Proteinuria (excess protein in the urine)
* Hematuria (blood in the urine)
* Reduced kidney function
* Swelling (edema)
* Joint pain
Lupus Nephritis can be diagnosed through a combination of physical examination, medical history, laboratory tests, and kidney biopsy. Treatment options for lupus nephritis include medications to suppress the immune system, control inflammation, and prevent further damage to the kidneys. In severe cases, dialysis or a kidney transplant may be necessary.
There are several key features of inflammation:
1. Increased blood flow: Blood vessels in the affected area dilate, allowing more blood to flow into the tissue and bringing with it immune cells, nutrients, and other signaling molecules.
2. Leukocyte migration: White blood cells, such as neutrophils and monocytes, migrate towards the site of inflammation in response to chemical signals.
3. Release of mediators: Inflammatory mediators, such as cytokines and chemokines, are released by immune cells and other cells in the affected tissue. These molecules help to coordinate the immune response and attract more immune cells to the site of inflammation.
4. Activation of immune cells: Immune cells, such as macrophages and T cells, become activated and start to phagocytose (engulf) pathogens or damaged tissue.
5. Increased heat production: Inflammation can cause an increase in metabolic activity in the affected tissue, leading to increased heat production.
6. Redness and swelling: Increased blood flow and leakiness of blood vessels can cause redness and swelling in the affected area.
7. Pain: Inflammation can cause pain through the activation of nociceptors (pain-sensing neurons) and the release of pro-inflammatory mediators.
Inflammation can be acute or chronic. Acute inflammation is a short-term response to injury or infection, which helps to resolve the issue quickly. Chronic inflammation is a long-term response that can cause ongoing damage and diseases such as arthritis, asthma, and cancer.
There are several types of inflammation, including:
1. Acute inflammation: A short-term response to injury or infection.
2. Chronic inflammation: A long-term response that can cause ongoing damage and diseases.
3. Autoimmune inflammation: An inappropriate immune response against the body's own tissues.
4. Allergic inflammation: An immune response to a harmless substance, such as pollen or dust mites.
5. Parasitic inflammation: An immune response to parasites, such as worms or fungi.
6. Bacterial inflammation: An immune response to bacteria.
7. Viral inflammation: An immune response to viruses.
8. Fungal inflammation: An immune response to fungi.
There are several ways to reduce inflammation, including:
1. Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying anti-rheumatic drugs (DMARDs).
2. Lifestyle changes, such as a healthy diet, regular exercise, stress management, and getting enough sleep.
3. Alternative therapies, such as acupuncture, herbal supplements, and mind-body practices.
4. Addressing underlying conditions, such as hormonal imbalances, gut health issues, and chronic infections.
5. Using anti-inflammatory compounds found in certain foods, such as omega-3 fatty acids, turmeric, and ginger.
It's important to note that chronic inflammation can lead to a range of health problems, including:
3. Heart disease
5. Alzheimer's disease
6. Parkinson's disease
7. Autoimmune disorders, such as lupus and rheumatoid arthritis.
Therefore, it's important to manage inflammation effectively to prevent these complications and improve overall health and well-being.
There are three main forms of ACH:
1. Classic congenital adrenal hyperplasia (CAH): This is the most common form of ACH, accounting for about 90% of cases. It is caused by mutations in the CYP21 gene, which codes for an enzyme that converts cholesterol into cortisol and aldosterone.
2. Non-classic CAH (NCAH): This form of ACH is less common than classic CAH and is caused by mutations in other genes involved in cortisol and aldosterone production.
3. Mineralocorticoid excess (MOE) or glucocorticoid deficiency (GD): These are rare forms of ACH that are characterized by excessive production of mineralocorticoids (such as aldosterone) or a deficiency of glucocorticoids (such as cortisol).
The symptoms of ACH can vary depending on the specific form of the disorder and the age at which it is diagnosed. In classic CAH, symptoms typically appear in infancy and may include:
* Premature puberty (in girls) or delayed puberty (in boys)
* Abnormal growth patterns
* Distended abdomen
* Weight gain or obesity
* Easy bruising or bleeding
In NCAH and MOE/GD, symptoms may be less severe or may not appear until later in childhood or adulthood. They may include:
* High blood pressure
* Low blood sugar (hypoglycemia)
* Weight gain or obesity
* Mood changes
If left untreated, ACH can lead to serious complications, including:
* Adrenal gland insufficiency
* Heart problems
* Bone health problems
* Increased risk of infections
* Mental health issues (such as depression or anxiety)
Treatment for ACH typically involves hormone replacement therapy to restore the balance of hormones in the body. This may involve taking medications such as cortisol, aldosterone, or other hormones to replace those that are deficient or imbalanced. In some cases, surgery may be necessary to remove an adrenal tumor or to correct physical abnormalities.
With proper treatment, many individuals with ACH can lead healthy, active lives. However, it is important for individuals with ACH to work closely with their healthcare providers to manage their condition and prevent complications. This may involve regular check-ups, hormone level monitoring, and lifestyle changes such as a healthy diet and regular exercise.
Proteinuria is usually diagnosed by a urine protein-to-creatinine ratio (P/C ratio) or a 24-hour urine protein collection. The amount and duration of proteinuria can help distinguish between different underlying causes and predict prognosis.
Proteinuria can have significant clinical implications, as it is associated with increased risk of cardiovascular disease, kidney damage, and malnutrition. Treatment of the underlying cause can help reduce or eliminate proteinuria.
There are two main types of MD:
1. Dry Macular Degeneration (DMD): This is the most common form of MD, accounting for about 90% of cases. It is caused by the gradual accumulation of waste material in the macula, which can lead to cell death and vision loss over time.
2. Wet Macular Degeneration (WMD): This type of MD is less common but more aggressive, accounting for about 10% of cases. It occurs when new blood vessels grow underneath the retina, leaking fluid and causing damage to the macula. This can lead to rapid vision loss if left untreated.
The symptoms of MD can vary depending on the severity and type of the condition. Common symptoms include:
* Blurred vision
* Distorted vision (e.g., straight lines appearing wavy)
* Difficulty reading or recognizing faces
* Difficulty adjusting to bright light
* Blind spots in central vision
MD can have a significant impact on daily life, making it difficult to perform everyday tasks such as driving, reading, and recognizing faces.
There is currently no cure for MD, but there are several treatment options available to slow down the progression of the disease and manage its symptoms. These include:
* Anti-vascular endothelial growth factor (VEGF) injections: These medications can help prevent the growth of new blood vessels and reduce inflammation in the macula.
* Photodynamic therapy: This involves the use of a light-sensitive drug and low-intensity laser to damage and shrink the abnormal blood vessels in the macula.
* Vitamin supplements: Certain vitamins, such as vitamin C, E, and beta-carotene, have been shown to slow down the progression of MD.
* Laser surgery: This can be used to reduce the number of abnormal blood vessels in the macula and improve vision.
It is important for individuals with MD to receive regular monitoring and treatment from an eye care professional to manage their condition and prevent complications.
There are several types of disease susceptibility, including:
1. Genetic predisposition: This refers to the inherent tendency of an individual to develop a particular disease due to their genetic makeup. For example, some families may have a higher risk of developing certain diseases such as cancer or heart disease due to inherited genetic mutations.
2. Environmental susceptibility: This refers to the increased risk of developing a disease due to exposure to environmental factors such as pollutants, toxins, or infectious agents. For example, someone who lives in an area with high levels of air pollution may be more susceptible to developing respiratory problems.
3. Lifestyle susceptibility: This refers to the increased risk of developing a disease due to unhealthy lifestyle choices such as smoking, lack of exercise, or poor diet. For example, someone who smokes and is overweight may be more susceptible to developing heart disease or lung cancer.
4. Immune system susceptibility: This refers to the increased risk of developing a disease due to an impaired immune system. For example, people with autoimmune disorders such as HIV/AIDS or rheumatoid arthritis may be more susceptible to opportunistic infections.
Understanding disease susceptibility can help healthcare providers identify individuals who are at risk of developing certain diseases and provide preventive measures or early intervention to reduce the risk of disease progression. Additionally, genetic testing can help identify individuals with a high risk of developing certain diseases, allowing for earlier diagnosis and treatment.
In summary, disease susceptibility refers to the predisposition of an individual to develop a particular disease or condition due to various factors such as genetics, environment, lifestyle choices, and immune system function. Understanding disease susceptibility can help healthcare providers identify individuals at risk and provide appropriate preventive measures or early intervention to reduce the risk of disease progression.
There are several symptoms of RA, including:
1. Joint pain and stiffness, especially in the hands and feet
2. Swollen and warm joints
3. Redness and tenderness in the affected areas
4. Fatigue, fever, and loss of appetite
5. Loss of range of motion in the affected joints
6. Firm bumps of tissue under the skin (rheumatoid nodules)
RA can be diagnosed through a combination of physical examination, medical history, blood tests, and imaging studies such as X-rays or ultrasound. Treatment typically involves a combination of medications, including nonsteroidal anti-inflammatory drugs (NSAIDs), disease-modifying anti-rheumatic drugs (DMARDs), and biologic agents. Lifestyle modifications such as exercise and physical therapy can also be helpful in managing symptoms and improving quality of life.
There is no cure for RA, but early diagnosis and aggressive treatment can help to slow the progression of the disease and reduce symptoms. With proper management, many people with RA are able to lead active and fulfilling lives.
Explanation: Genetic predisposition to disease is influenced by multiple factors, including the presence of inherited genetic mutations or variations, environmental factors, and lifestyle choices. The likelihood of developing a particular disease can be increased by inherited genetic mutations that affect the functioning of specific genes or biological pathways. For example, inherited mutations in the BRCA1 and BRCA2 genes increase the risk of developing breast and ovarian cancer.
The expression of genetic predisposition to disease can vary widely, and not all individuals with a genetic predisposition will develop the disease. Additionally, many factors can influence the likelihood of developing a particular disease, such as environmental exposures, lifestyle choices, and other health conditions.
Inheritance patterns: Genetic predisposition to disease can be inherited in an autosomal dominant, autosomal recessive, or multifactorial pattern, depending on the specific disease and the genetic mutations involved. Autosomal dominant inheritance means that a single copy of the mutated gene is enough to cause the disease, while autosomal recessive inheritance requires two copies of the mutated gene. Multifactorial inheritance involves multiple genes and environmental factors contributing to the development of the disease.
Examples of diseases with a known genetic predisposition:
1. Huntington's disease: An autosomal dominant disorder caused by an expansion of a CAG repeat in the Huntingtin gene, leading to progressive neurodegeneration and cognitive decline.
2. Cystic fibrosis: An autosomal recessive disorder caused by mutations in the CFTR gene, leading to respiratory and digestive problems.
3. BRCA1/2-related breast and ovarian cancer: An inherited increased risk of developing breast and ovarian cancer due to mutations in the BRCA1 or BRCA2 genes.
4. Sickle cell anemia: An autosomal recessive disorder caused by a point mutation in the HBB gene, leading to defective hemoglobin production and red blood cell sickling.
5. Type 1 diabetes: An autoimmune disease caused by a combination of genetic and environmental factors, including multiple genes in the HLA complex.
Understanding the genetic basis of disease can help with early detection, prevention, and treatment. For example, genetic testing can identify individuals who are at risk for certain diseases, allowing for earlier intervention and preventive measures. Additionally, understanding the genetic basis of a disease can inform the development of targeted therapies and personalized medicine."
The disorder is caused by mutations in the HBB gene that codes for the beta-globin subunit of hemoglobin. These mutations result in the production of abnormal hemoglobins that are unstable and prone to breakdown, leading to the release of free hemoglobin into the urine.
HP is classified into two types based on the severity of symptoms:
1. Type 1 HP: This is the most common form of the disorder and is characterized by mild to moderate anemia, occasional hemoglobinuria, and a normal life expectancy.
2. Type 2 HP: This is a more severe form of the disorder and is characterized by severe anemia, recurrent hemoglobinuria, and a shorter life expectancy.
There is no cure for HP, but treatment options are available to manage symptoms and prevent complications. These may include blood transfusions, folic acid supplements, and medications to reduce the frequency and severity of hemoglobinuria episodes.
The term "immune complex disease" was first used in the 1960s to describe a group of conditions that were thought to be caused by the formation of immune complexes. These diseases include:
1. Systemic lupus erythematosus (SLE): an autoimmune disorder that can affect multiple organ systems and is characterized by the presence of anti-nuclear antibodies.
2. Rheumatoid arthritis (RA): an autoimmune disease that causes inflammation in the joints and can lead to joint damage.
3. Type III hypersensitivity reaction: a condition in which immune complexes are deposited in tissues, leading to inflammation and tissue damage.
4. Pemphigus: a group of autoimmune diseases that affect the skin and mucous membranes, characterized by the presence of autoantibodies against desmosomal antigens.
5. Bullous pemphigoid: an autoimmune disease that affects the skin and is characterized by the formation of large blisters.
6. Myasthenia gravis: an autoimmune disorder that affects the nervous system, causing muscle weakness and fatigue.
7. Goodpasture's syndrome: a rare autoimmune disease that affects the kidneys and lungs, characterized by the presence of immune complexes in the glomeruli of the kidneys.
8. Hemolytic uremic syndrome (HUS): a condition in which red blood cells are destroyed and waste products accumulate in the kidneys, leading to kidney failure.
Immune complex diseases can be caused by various factors, including genetic predisposition, environmental triggers, and exposure to certain drugs or toxins. Treatment options for these diseases include medications that suppress the immune system, such as corticosteroids and immunosuppressive drugs, and plasmapheresis, which is a process that removes harmful antibodies from the blood. In some cases, organ transplantation may be necessary.
In conclusion, immune complex diseases are a group of disorders that occur when the body's immune system mistakenly attacks its own tissues and organs, leading to inflammation and damage. These diseases can affect various parts of the body, including the skin, kidneys, lungs, and nervous system. Treatment options vary depending on the specific disease and its severity, but may include medications that suppress the immune system and plasmapheresis.
Complement receptor 1
Complement control protein
Complement receptor 2
Laminin subunit alpha-1
Complement component 3
List of MeSH codes (D12.776.124)
Mixed autoimmune hemolytic anemia
Autoimmune hemolytic anemia
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RESEARCHER OF THE MONTH August 2017 - Johannes Hofer
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- When CR2 is bound by its primary C3 activation fragment-derived ligand , designated C3d, it coassociates with CD19 on B cells to amplify BCR signaling. (bvsalud.org)
- 13. The complement fragment C3d facilitates phagocytosis by monocytes. (nih.gov)
- Dr. Johannes Hofer was selected MedUni Vienna Researcher of the Month, August 2017, for the work „Ig-like transcript 4 as a cellular receptor for soluble complement fragment C4d", published in „FASEB Journal" (IF 5.5). (meduniwien.ac.at)
- The smaller fragment formed when complement C4 is cleaved by COMPLEMENT C1S. (lookformedical.com)
- The smaller fragment generated from the cleavage of complement C3 by C3 CONVERTASE. (lookformedical.com)
- The minor fragment formed when C5 convertase cleaves C5 into C5a and COMPLEMENT C5B. (lookformedical.com)
- The major fragment C5b binds to the membrane initiating the spontaneous assembly of the late complement components, C5-C9, into the MEMBRANE ATTACK COMPLEX. (lookformedical.com)
- Analysis of Protein Array containing more than 19,000 full-length human proteins using Complement C3d-Monospecific Mouse Monoclonal Antibody (C3D/2891). (neobiotechnologies.com)
- The complement component proteins, C2, C3, C4 and C5, are potent anaphylatoxins that are released during complement activation. (neobiotechnologies.com)
- Genes that encode the proteins of complement components or their isotypes are distributed throughout different chromosomes, with 19 genes comprising 3 significant complement gene clusters in the human genome. (medscape.com)
- The important components of this system are various cell membrane-associated proteins such as complement receptor 1 (CR1), complement receptor 2 (CR2), and decay accelerating factor (DAF). (medscape.com)
- Global pathway analysis by Ingenuity software highlighted the presence of several circulating proteins, among them were proteins from the complement system. (elsevier.com)
- Special Complements Research Reagents are products that are used for the analysis of the complement system, a part of the immune system that consists of a series of proteins that can be activated by various stimuli. (immunoconceptindia.co)
- These kits allow for the analysis of activation of key proteins and specific pathways of the complement system in serum, plasma, and other biological fluids. (immunoconceptindia.co)
- Purified antigens might have contaminants, or might not contain the full complement of native proteins. (bmj.com)
- The complement control protein (CCP) modules (also known as short consensus repeats SCRs or SUSHI repeats) contain approximately 60 amino acid residues and have been identified in several proteins of the complement system. (embl.de)
- These modules have been identified more than 140 times in over 20 proteins, including 12 proteins of the complement system. (embl.de)
- The complement system is a group of proteins that work together to destroy foreign invaders (such as bacteria and viruses), trigger inflammation, and remove debris from cells and tissues. (medlineplus.gov)
- One of these pieces, called C3b, interacts with several other proteins on the surface of cells to trigger the complement system's response. (medlineplus.gov)
- 4. Phagocytosis of Mycobacterium leprae by human monocyte-derived macrophages is mediated by complement receptors CR1 (CD35), CR3 (CD11b/CD18), and CR4 (CD11c/CD18) and IFN-gamma activation inhibits complement receptor function and phagocytosis of this bacterium. (nih.gov)
- 7. Modulation of complement receptors of a human monocyte cell line, U-937, during incubation with phorbol myristate acetate: expression of an iC3b-specific receptor (CR3). (nih.gov)
- 12. Development of functional complement receptors during in vitro maturation of human monocytes into macrophages. (nih.gov)
- 14. Defective complement receptors (CR1 and CR3) on erythrocytes and leukocytes of factor I (C3b-inactivator) deficient patients. (nih.gov)
- Location of binding sites in the C3 fragments for factors B and H, complement receptors, and bovine conglutinin. (nih.gov)
- 20. Phagocytosis of Mycobacterium tuberculosis is mediated by human monocyte complement receptors and complement component C3. (nih.gov)
- However, C4d did not bind to classic complement receptors. (meduniwien.ac.at)
- Receptors, Complement" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (harvard.edu)
- This graph shows the total number of publications written about "Receptors, Complement" by people in Harvard Catalyst Profiles by year, and whether "Receptors, Complement" was a major or minor topic of these publication. (harvard.edu)
- Below are the most recent publications written about "Receptors, Complement" by people in Profiles. (harvard.edu)
- Untangling Fc and complement receptors to kill tumors. (harvard.edu)
- C3d is a terminal degradation product of C3 that plays an important role in modulation of the adaptive immune response through the interaction with complement receptor type 2 (CR2). (neobiotechnologies.com)
- Complement receptor type 2 (CR2)/CD21 plays a key role in the development of high-affinity Abs and long-lasting memory to foreign Ags. (bvsalud.org)
- 3. Membrane complement receptor type three (CR3) has lectin-like properties analogous to bovine conglutinin as functions as a receptor for zymosan and rabbit erythrocytes as well as a receptor for iC3b. (nih.gov)
- 6. Identification of an anti-monocyte monoclonal antibody that is specific for membrane complement receptor type one (CR1). (nih.gov)
- The CD21 antigen is also known as complement receptor type 2 (CR2), C3d receptor, and Epstein-Barr virus receptor (EBV-R). (bdbiosciences.com)
- SDS-PAGE Analysis Purified Complement 3d Mouse Monoclonal Antibody (C3D/2891). (neobiotechnologies.com)
- Formalin-fixed, paraffin-embedded human rejected kidney transplant stained with Complement 3d Mouse Monoclonal Antibody (C3D/2891) at 2ug/ml in PBS. (neobiotechnologies.com)
- Lectins activate the lectin pathway in a manner similar to the antibody interaction with complement in the classical pathway. (medscape.com)
- Complement regulation leads to the generation of complement split products such as complement component (C)4d, a marker for disease activity in autoimmune syndromes or antibody-mediated allograft rejection. (meduniwien.ac.at)
- Both the activating and inhibitory Fc γ Rs and the activation of different complement cascades contribute to the downstream effector functions in the antibody-mediated disease pathology. (hindawi.com)
- Finally, the functional role of local complement activation in polymorphonuclear (PMN) cell activation was tested, showing that C3 blockade by anti-C3 antibody was able to decrease thrombus-induced neutrophil chemotaxis and reactive oxygen species production. (elsevier.com)
- The anti-complement component consists of murine monoclonal IgG anti-C3d-antibody reactive with C3b and C3d-coated red blood cells. (bio-rad.com)
- Reaction to the specified food will worsen if C3d activation is present along with an IgG antibody response. (drjockers.com)
- Factors initiating complement activation include ANTIGEN-ANTIBODY COMPLEXES, microbial ANTIGENS, or cell surface POLYSACCHARIDES. (lookformedical.com)
- It is generated when C3b is inactivated (iC3b) and its alpha chain is cleaved by COMPLEMENT FACTOR I into C3c, and C3dg (955-1303) in the presence COMPLEMENT FACTOR H . Serum proteases further degrade C3dg into C3d (1002-1303) and C3g (955-1001). (nih.gov)
- CD21, also known as CR2 (complement receptor 2) and C3d receptor, binds C3d and iC3b. (biolegend.com)
- Se genera cuando se inactiva C3b (iC3b) y su cadena alfa es desdoblada por el FACTOR I DEL COMPLEMENTO en C3c y C3dg (955-1303) en presencia del FACTOR H DEL COMPLEMENTO. (bvsalud.org)
- It is generated when C3b is inactivated (iC3b) and its alpha chain is cleaved by COMPLEMENT FACTOR I into C3c (749-954), and C3dg (955-1303) in the presence COMPLEMENT FACTOR H. (lookformedical.com)
- Acts also in the inhibition of spontaneous complement activation by impairing the formation and function of the alternative and classical pathway C3/C5 convertases, and by serving as a cofactor for the cleavage by factor I of C3b to iC3b, C3c and C3d,g, and of C4b to C4c and C4d (PubMed:2972794, PubMed:8175757). (nih.gov)
- IH-Card containing rabbit Anti-IgG and monoclonal Anti-C3d. (bio-rad.com)
- Las proteasas séricas degradan aún más C3dg en C3d (1002-1303) y C3g (955-1001). (bvsalud.org)
- Direct and indirect immunofluorescence and immunoperoxidase assays showed colocalization along the myelin sheaths of peripheral-nerve fibers of monoclonal protein with complement components C1q, C3d, and C5. (nih.gov)
- In addition, terminal-complement complex that was not associated with S protein was detected in myelin sheaths. (nih.gov)
- Identification of a 145,000 Mr membrane protein as the C3d receptor (CR2) of human B lymphocytes. (bdbiosciences.com)
- The sushi domain is also known as the complement controle protein (CCP) module or the short consensus repeat (SCR). (embl.de)
- Three-dimensional structure of a complement control protein module in solution. (embl.de)
- The complement control protein (CCP) modules (also known as short consensus repeats) are defined by a consensus sequence within a stretch of about 60 amino acid residues. (embl.de)
- The C3 gene provides instructions for making a protein called complement component 3 (or C3). (medlineplus.gov)
- This protein plays a key role in a part of the body's immune response known as the complement system. (medlineplus.gov)
- The C3 protein is essential for turning on (activating) the complement system. (medlineplus.gov)
- This genetic change is described as a "gain-of-function" mutation because it leads to an altered version of the protein that overactivates the complement system. (medlineplus.gov)
- These mutations are described as "loss-of-function" because the abnormal or missing C3 protein prevents normal activation of the complement system. (medlineplus.gov)
- Complement factor D (CFD), a rate limiting component of the alternative pathway of complement activation and the complement activation products C5a and C3d were determined in the plasma samples by ELISA. (nih.gov)
- A glycoprotein that is central in both the classical and the alternative pathway of COMPLEMENT ACTIVATION. (lookformedical.com)
- It is a constituent of the ALTERNATIVE PATHWAY C3 CONVERTASE (C3bBb), and COMPLEMENT C5 CONVERTASES in both the classical (C4b2a3b) and the alternative (C3bBb3b) pathway. (lookformedical.com)
- 8. gp140, a C3b-binding membrane component of lymphocytes, is the B cell C3dg/C3d receptor (CR2) and is distinct from the neutrophil C3dg receptor (CR4). (nih.gov)
- It was observed that the escape variants carried covalently bound complement activation fragments, especially C3d. (nih.gov)
- Whether lutein also affects activation of the complement system has not yet been addressed and was the purpose of the study described here. (nih.gov)
- at the same time, the inflammation promoted by complement activation can result in cellular damage when not kept in check. (medscape.com)
- CONCLUSIONS - : A decrease of systemic C3 concentration and activity in the later stages of AAA associated with local complement retention, consumption, and proteolysis in the thrombus could induce PMN chemotaxis and activation, playing a detrimental role in AAA progression. (elsevier.com)
- The Dietary Antigen Test (IgG with Complement) measures Complement activation for multiple foods. (drjockers.com)
- Complement activation is well-defined in the research as not only a cause of inflammation but one of the strongest causes. (drjockers.com)
- Also, 57 of 60 metabolites were associated significantly with complement activation levels, independent of AMD status. (ucl.ac.uk)
- Increased large and extra-large HDL levels and decreased VLDL and amino acid levels were associated with increased complement activation. (ucl.ac.uk)
- We observed strong associations between the vast majority of the AMD-associated metabolites and systemic complement activation levels, independent of AMD status. (ucl.ac.uk)
- This complex is arranged in nine subunits (six disulfide-linked dimers of A and B, and three disulfide-linked homodimers of C). C1q has binding sites for antibodies (the heavy chain of IMMUNOGLOBULIN G or IMMUNOGLOBULIN M). The interaction of C1q and immunoglobulin activates the two proenzymes COMPLEMENT C1R and COMPLEMENT C1S, thus initiating the cascade of COMPLEMENT ACTIVATION via the CLASSICAL COMPLEMENT PATHWAY. (lookformedical.com)
- Serum glycoproteins participating in the host defense mechanism of COMPLEMENT ACTIVATION that creates the COMPLEMENT MEMBRANE ATTACK COMPLEX. (lookformedical.com)
- The complement cascade consists of 3 separate pathways that converge in a final common pathway. (medscape.com)
- Complement pathways and deficiencies. (medscape.com)
- PURPOSE: The current study aimed to identify metabolites associated with age-related macular degeneration (AMD) by performing the largest metabolome association analysis in AMD to date, as well as aiming to determine the effect of AMD-associated genetic variants on metabolite levels and investigate associations between the identified metabolites and activity of the complement system, one of the main AMD-associated disease pathways. (ucl.ac.uk)
- An Alternative Complement Pathway, Rat, Assay ELISA Kit is a type of assay kit that can measure the activity of the alternative complement pathway in rat serum or plasma samples. (immunoconceptindia.co)
- A Classical Complement Pathway, Mouse, Assay ELISA Kit is a type of ELISA kit that can measure the activity of the classical complement pathway in mouse serum or plasma samples. (immunoconceptindia.co)
Defined the role of complement1
- Cases of complement deficiency have helped defined the role of complement in host defense. (medscape.com)
- Role of complement-binding CD21/CD19/CD81 in enhancing human B cell protection from Fas-mediated apoptosis. (bdbiosciences.com)
- C6 is the next complement component to bind to the membrane-bound COMPLEMENT C5B in the assembly of MEMBRANE ATTACK COMPLEX. (lookformedical.com)
- Impact of the common genetic associations of age-related macular degeneration upon systemic complement component C3d levels. (cdc.gov)
- Here, the authors tested the efficacy of the DNA epitope vaccine p3Abeta 1-11-PADRE and the same vaccine fused with a component of complement 3C3d (p3Abeta 1-11-PADRE-3C3d) in a transgenic (Tg) mouse model of AD (Tg2576), of the H2bxs immune haplotype. (nih.gov)
- When C3d is activated in response to an antigen, the C3 portion attaches to the antigen. (drjockers.com)
- Membrane immune adherence receptor that plays a critical role in the capture and clearance of complement-opsonized pathogens by erythrocytes and monocytes/macrophages (PubMed:2963069). (nih.gov)
- Molecules on the surface of some B-lymphocytes and macrophages, that recognize and combine with the C3b, C3d, C1q, and C4b components of complement. (harvard.edu)
- However, prior studies in murine models of SLE using gene -targeted Cr2-/- mice , which lack both CR2 and complement receptor 1 (CR1), have demonstrated contradictory results. (bvsalud.org)
- Evaluating the Occurrence of Rare Variants in the Complement Factor H Gene in Patients With Early-Onset Drusen Maculopathy. (cdc.gov)
- C3d is an activator of the Complement cascade system. (drjockers.com)
- In addition to playing an important role in host defense against infection, the complement system is a mediator in both the pathogenesis and prevention of immune complex diseases, such as systemic lupus erythematosus (SLE). (medscape.com)
- We investigated the role of complement in the pathogenesis of the demyelinating polyneuropathy that occurs in some patients with IgM monoclonal gammopathy. (nih.gov)
- NIH inventors have generated several C3d-specific mouse and rabbit monoclonal antibodies to re-target cells that have escaped from mAb therapy. (nih.gov)
Adaptive immune r1
- New studies point to the complex interplay between the complement cascade and adaptive immune response, and complement is also being studied in association with ischemic injury as a target of therapy. (medscape.com)
- Complement Technology Laboratories manufactures the complement technolo reagents distributed by Genprice. (nexeonmedsystems.com)
- Targeting the Immune Complex-Bound Complement C3d Ligand as a Novel Therapy for Lupus. (bvsalud.org)
- C3d and CR2 also mediate immune complex binding to follicular dendritic cells . (bvsalud.org)
- As the development of SLE involves subversion of normal B cell tolerance checkpoints, one might expect that CR2 ligation by C3d-bound immune complexes would promote development of SLE. (bvsalud.org)
- The complement system is part of the innate immune system. (medscape.com)
- Mediates the binding by these cells of particles and immune complexes that have activated complement to eliminate them from the circulation (PubMed:2963069). (nih.gov)
- With this novel tool, we show that disruption of the critical C3d-CR2 ligand -receptor binding step alone substantially ameliorates autoimmunity and renal disease in the MRL/lpr model of SLE. (bvsalud.org)
- C3 can be cleaved into COMPLEMENT C3A and COMPLEMENT C3B, spontaneously at low level or by C3 CONVERTASE at high level. (lookformedical.com)
- Deficiencies in the complement cascade can lead to overwhelming infection and sepsis. (medscape.com)
- Complement deficiencies are said to comprise between 1 and 10% of all primary immunodeficiencies. (medscape.com)
- [ 4 ] A registry of complement deficiencies has been established as a means to promote joint projects on treatment and prevention of diseases associated with defective complement function. (medscape.com)
- This article outlines some of the disease states associated with complement deficiencies and their clinical implications. (medscape.com)
- Deficiencies in complement predispose patients to infection via 2 mechanisms: (1) ineffective opsonization and (2) defects in lytic activity (defects in MAC). (medscape.com)
- Specific complement deficiencies are also associated with an increased risk of developing autoimmune disease, such as SLE. (medscape.com)
- Vaccinate patients against encapsulated bacteria at least 2 weeks prior to initiation of ENJAYMO therapy according to the most current Advisory Committee on Immunization Practices (ACIP) recommendations for patients with persistent complement deficiencies [see Warnings and Precautions (5.1) ]. (nih.gov)
- This pH- and ionic strength-dependent association of C3d with CR2 represents a link between innate and adaptive immunity. (wlsolutions.be)
- Although the complement system is part of the body's innate, relatively nonspecific defense against pathogens, its role is hardly primitive or easily understood. (medscape.com)
- As a new approach, we developed a highly specific mouse anti- mouse C3d mAb that blocks its interaction with CR2. (bvsalud.org)
- 10. Differential requirements for cellular cytoskeleton in human macrophage complement receptor- and Fc receptor-mediated phagocytosis. (nih.gov)
- IH -Card AHG Anti-IgG,-C3d consists of six microtubes containing a gel impregnated with polyspecific Anti-Human Globulin (AHG) containing a blend of rabbit anti-IgG and murine monoclonal anti-complement. (bio-rad.com)
- A North African study of molecular basis of complement factor I deficiency in atypical hemolytic and uremic syndrome patients suggested that the Ile357Met mutation may be a founding effect. (medscape.com)
- The solution structure of the 16th CCP module from human complement factor H has been determined by a combination of 2-dimensional nuclear magnetic resonance spectroscopy and restrained simulated annealing. (embl.de)
- Dynamic regulation of B cell complement signaling is integral to germinal center responses. (harvard.edu)
- No association of a combination of single-nucleotide polymorphisms in complement genes between large and small AAA patients was observed. (elsevier.com)
- The complement system plays an important part in defense against pyogenic organisms. (medscape.com)
- These findings underscore the duality of the complement system. (medscape.com)
- Knowledge about the complement system is expanding. (medscape.com)
- An intricate system regulates complement activity. (medscape.com)
- The complex functioning of the complement system in xenotransplantation. (harvard.edu)
- Breaking down the complement system: a review and update on novel therapies. (harvard.edu)
- This process must be carefully regulated so the complement system targets only unwanted materials and does not damage the body's healthy cells. (medlineplus.gov)
- It appeared that alterations in myelin geometry caused by the separation of myelin lamellae corresponded to sites at which terminal-complement complex was deposited. (nih.gov)