Complement System Proteins
Anaplasma marginale
Complement Activation
Phosphotransferases (Nitrogenous Group Acceptor)
Complement C3
Phosphoenolpyruvate Sugar Phosphotransferase System
Complement C4
Complement Pathway, Classical
Complement Pathway, Alternative
Complement C5
Complement Inactivator Proteins
Complement C3b
Complement Factor B
Complement C1q
Complement C3a
Complement Membrane Attack Complex
Receptors, Complement
Complement C2
Complement C5a
Anaphylatoxins
Gene Expression Regulation, Bacterial
Complement C4b
Complement Inactivating Agents
Complement C9
Complement Hemolytic Activity Assay
Complement C1
Complement Factor H
Complement C3-C5 Convertases
Complement C6
Complement Activating Enzymes
Complement C3d
Complement C4a
Receptors, Complement 3b
Complement C3c
Complement Factor I
Complement C1 Inhibitor Protein
Receptor, Anaphylatoxin C5a
Complement Factor D
Antigens, CD55
Complement C1 Inactivator Proteins
Complement Pathway, Mannose-Binding Lectin
Mannose-Binding Protein-Associated Serine Proteases
Cobra Venoms
Complement C8
Complement C4b-Binding Protein
Complement C3b Inactivator Proteins
Hemolysis
Complement C7
Mannose-Binding Lectin
Receptors, Complement 3d
Complement Fixation Tests
Antigens, CD59
Properdin
Antigens, CD46
Complement C1s
Complement C1r
Complement C5b
Complement C2b
Complement C3 Convertase, Alternative Pathway
Opsonin Proteins
Collectins
Antigen-Antibody Complex
Immunoglobulin G
Lectins
Blood Bactericidal Activity
Phthalic Anhydrides
Phagocytosis
Immunity, Innate
Guinea Pigs
Molecular Sequence Data
Neutrophils
Immunoelectrophoresis
Amino Acid Sequence
Protein Binding
Sarcoptes scabiei
gamma-Globulins
Snake Venoms
Macular Degeneration
Forssman Antigen
Serum
Erythrocytes
Veillonella
Bothrops
Rabbits
Macrophage-1 Antigen
Immunoglobulin M
Oxyphenbutazone
Antibodies
Blood Proteins
Integrin alphaXbeta2
Immune Complex Diseases
Immunodiffusion
Dose-Response Relationship, Immunologic
Mice, Knockout
Enzyme-Linked Immunosorbent Assay
Serine Endopeptidases
Immune Adherence Reaction
Complement C3 Nephritic Factor
Inflammation
Disease Models, Animal
Sheep
Venoms
Glycoproteins
Hemolytic-Uremic Syndrome
Genetic Complementation Test
Urochordata
Kaolin
Arthropod Proteins
Antigen-Antibody Reactions
Surface Plasmon Resonance
Base Sequence
Leukocytes
Lipopolysaccharides
Peptide Fragments
Endotoxins
Mutation
Protein S
Immune Sera
Chemotaxis, Leukocyte
Cells, Cultured
Lupus Erythematosus, Systemic
Mannose
Sepsis
Reperfusion Injury
Fluorescent Antibody Technique
Macrophages
Blood Coagulation
Antigens, CD
Carrier Proteins
RNA, Messenger
Binding Sites
Electrophoresis, Polyacrylamide Gel
Immunoglobulins
Species Specificity
Immune System
C-Reactive Protein
Anaphylaxis
Protein Structure, Tertiary
Histocompatibility Antigens
Peptides, Cyclic
Cloning, Molecular
Escherichia coli
Liver
Shock, Septic
Peptide Hydrolases
Interaction of inflammatory cells and oral microorganisms. III. Modulation of rabbit polymorphonuclear leukocyte hydrolase release response to Actinomyces viscosus and Streptococcus mutans by immunoglobulins and complement. (1/3896)
In the absence of antiserum, rabbit polymorphonuclear leukocytes (PMNs) released lysosomal enzymes in response to Actinomyces viscosus (19246) but not to Streptococcus mutans (6715). Antibodies had a marked modulating influence on these reactions. PMN hydrolase release was significantly enhanced to both organisms when specific rabbit antiserum and isolated immunoglobulin G (IgG) were included in the incubations. Immune complex F(ab')2 fragments of IgG directed against S. mutans agglutinated bacteria. Immune complexes consisting of S. mutans and F(ab')2 fragments of IgG directed against this organism were not effective as bacteria-IgG complexes in stimulating PMN release. The intensity of the release response to bacteria-IgG complexes was also diminished when PMNs were preincubated with isolated Fc fragments derived from IgG. Fresh serum as a source of complement components had no demonstrable effect on PMN release either alone or in conjuction with antiserum in these experiments. These data may be relevant to the mechanisms and consequences of the interaction of PMNs and plaque bacteria in the pathogenesis of periodontal disease. (+info)Up-regulation of glomerular extracellular matrix and transforming growth factor-beta expression in RF/J mice. (2/3896)
BACKGROUND: RF/J mice were first reported as a murine model of spontaneous glomerulosclerosis by Gude and Lupton in 1960, but the precise histologic characteristics and immunopathological background of this mouse have not been investigated further. METHODS: Measurements of serum levels of immunoglobulins, anti-single strand DNA (anti-ss-DNA) antibody, complement (C3), and circulating immune complex (IC) were performed. Analyses of glomerular histological and immunopathological lesions in association with the detection of mRNA expression of collagen IV, TGF-beta, matrix protein turnover related enzymes, matrix metalloproteinase-2 (MMP-2), tissue inhibitor of metalloproteinase-2 (TIMP-2) and platelet-derived growth factor (PDGF) were also performed in young (10-week-old) and elderly (60-week-old) RF/J mice with age-matched BALB/C mice as the controls. RESULTS: High levels of serum IgA and IgG from as early as 20 weeks of age were noted in the RF/J mice. Serum anti-ss-DNA antibody of aged RF/J mice increased up to 23% of that of aged MRL-lpr/lpr mice, and serum C3 concentration significantly decreased with age, reaching lower levels than that of BALB/c mice. IgA-IC levels were significantly high compared to BALB/C mice both in the early and late stages of life, whereas IgG-IC levels were high only in mice younger than 20 weeks. Semiquantitative and quantitative analyzes of renal histopathological findings revealed significantly marked and age-related mesangial matrix expansion in RF/J mice, with increasing frequency of global glomerular sclerosis and tubulointerstitial damage. On the other hand, although precise measurements of glomerular cell numbers also showed an apparent augmentation in both young and old RF/J mice compared to BALB/C mice, glomerular cellularity decreased with age in RF/J mice. Immunohistochemical study revealed massive immunoglobulin deposition from a young age in association with significantly higher accumulation of matrix proteins, such as types I and IV collagen and laminin from the early stage of life. In addition, in these glomeruli, transforming growth factor-beta1 (TGF-beta1) was highly expressed both in young and old mice. The mRNA expression of MMP-2 was up-regulated only in the early stage of life. Although PDGF mRNA of RF/J mice was significantly up-regulated in the early stage of life, the differences between the mice disappeared in the late stage of life. CONCLUSIONS: These findings suggest that in RF/J mice, an immunopathological background inducing high serum immunoglobulin and IC levels from the early stage of life is closely related to mesangioproliferative glomerular lesions mediated by PDGF, and that development of massive extracellular matrix accumulation in glomeruli was induced by up-regulated expression of TGF-beta with inappropriate regulation of protein turnover-related enzyme production. (+info)Assessment of complement deficiency in patients with meningococcal disease in The Netherlands. (3/3896)
The frequency of complement deficiency in 176 of 7,732 patients with meningococcal disease in the Netherlands from 1959 through 1992 was assessed. Complement deficiency was found in six patients (3%): 3 (7%) of the patients with Neisseria meningitidis serogroup C disease, 1 (2%) of the patients with N. meningitidis serogroup A disease, and 2 (33%) of the patients with infections due to uncommon serogroups and nongroupable strains of N. meningitidis. Of 91 additional patients with meningococcal infections due to uncommon serogroups, 33% also had complement deficiency. Thirty-four of the 36 complement-deficient patients with meningococcal disease who were from 33 families were 5 years of age or older. Twenty-six additional complement-deficient relatives were found. Screening individuals with meningococcal disease due to uncommon serogroups who were 5 years of age or older identified 30 of the 33 complement-deficient families. Only 27% of the complement-deficient relatives had had meningococcal disease. This risk was lower for relatives with properdin deficiency (18%) than for those deficient in the late component of complement (38%). Therefore, pedigree studies are warranted for identifying those complement-deficient persons who require vaccination for meningococcal disease. (+info)2-Deoxyglucose selectively inhibits Fc and complement receptor-mediated phagocytosis in mouse peritoneal macrophages II. Dissociation of the inhibitory effects of 2-deoxyglucose on phagocytosis and ATP generation. (4/3896)
Macrophages incubated in 2-deoxy-D-glucose (2-dG)-containing medium showed a marked decrease in cellular ATP content, and were unable to ingest IgG- and complement-coated erythrocytes via the corresponding membrane receptors for these ligands. However, the inhibitory effects of 2-dG on Fc- and C3 receptor-mediated phagocytosis were not a consequence of lowered macrophage ATP levels since addition of glucose or mannose to the culture medium restored the capacity of the macrophages to ingest IgG- and C3-coated particles without increasing ATP levels. These results indicate that Fc- and C3 receptor-mediated phagocytosis (opsonin dependent) differs qualitatively from the ingestion of latex and zymosan particles (opsonin independent); they suggest that the same regulatory molecules govern the responses of phagocytic cells to signals initiated by both the Fc and C3 receptors. The possibility that these molecules are regulated by glycosylation is discussed. (+info)The induction of macrophage spreading: role of coagulation factors and the complement system. (5/3896)
Unstimulated mouse peritoneal macrophages, attached to either glass or plastic substrates, responded to factors generated in serum and plasma by spreading and increasing their apparent surface area up to eightfold. Two distinct and dissociable systems were involved. The first appears related to the distinct and dissociable systems were involved. The first appears related to the contact phase of blood coagulation. It is activated by glass and not plastic surfaces, depleted by kaolin adsorption, and inhibited by soybean trypsin inhibitor. In contrast, a separate complement-dependent system can be generated in kaolin-adsorbed plasma. Activation of the complement system can occur either by the alternate or classical pathways and generates a relatively small effector molecule which is dialyzable. These factors presumably influencing the surface membrane and underlying structures may explain the rapid spreading of activated macrophages observed after both infections and chemical peritoneal inflammatory agents. (+info)Unexpected crucial role of residue 225 in serine proteases. (6/3896)
Residue 225 in serine proteases of the chymotrypsin family is Pro or Tyr in more than 95% of nearly 300 available sequences. Proteases with Y225 (like some blood coagulation and complement factors) are almost exclusively found in vertebrates, whereas proteases with P225 (like degradative enzymes) are present from bacteria to human. Saturation mutagenesis of Y225 in thrombin shows that residue 225 affects ligand recognition up to 60,000-fold. With the exception of Tyr and Phe, all residues are associated with comparable or greatly reduced catalytic activity relative to Pro. The crystal structures of three mutants that differ widely in catalytic activity (Y225F, Y225P, and Y225I) show that although residue 225 makes no contact with substrate, it drastically influences the shape of the water channel around the primary specificity site. The activity profiles obtained for thrombin also suggest that the conversion of Pro to Tyr or Phe documented in the vertebrates occurred through Ser and was driven by a significant gain (up to 50-fold) in catalytic activity. In fact, Ser and Phe are documented in 4% of serine proteases, which together with Pro and Tyr account for almost the entire distribution of residues at position 225. The unexpected crucial role of residue 225 in serine proteases explains the evolutionary selection of residues at this position and shows that the structural determinants of protease activity and specificity are more complex than currently believed. These findings have broad implications in the rational design of enzymes with enhanced catalytic properties. (+info)Phagocytosis of Vibrio cholerae O139 Bengal by human polymorphonuclear leukocytes. (7/3896)
Capsulated bacteria exhibit serum (complement) resistance and resistance to phagocytosis, which result in disseminated infections. Vibrio cholerae O139 strains possess a thin capsule and have been found to be partially serum resistant in a previous study. In the present study, compared to a standard capsulated Klebsiella pneumoniae strain, which showed total resistance to killing by phagocytosis, V. cholerae O139 strains were shown to be only partially resistant, with most strains showing <40% survival. These findings may explain the relative rarity of V. cholerae O139 bacteremia in cholera caused by this organism. (+info)Intestinal reperfusion injury is mediated by IgM and complement. (8/3896)
Intestinal ischemia-reperfusion injury is dependent on complement. This study examines the role of the alternative and classic pathways of complement and IgM in a murine model of intestinal ischemia-reperfusion. Wild-type animals, mice deficient in complement factor 4 (C4), C3, or Ig, or wild-type mice treated with soluble complement receptor 1 were subjected to 40 min of jejunal ischemia and 3 h of reperfusion. Compared with wild types, knockout and treated mice had significantly reduced intestinal injury, indicated by lowered permeability to radiolabeled albumin. When animals deficient in Ig were reconstituted with IgM, the degree of injury was restored to wild-type levels. Immunohistological staining of intestine for C3 and IgM showed colocalization in the mucosa of wild-type controls and minimal staining for both in the intestine of Ig-deficient and C4-deficient mice. We conclude that intestinal ischemia-reperfusion injury is dependent on the classic complement pathway and IgM. (+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.
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.
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.
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:
1. Arthritis
2. Diabetes
3. Heart disease
4. Cancer
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.
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.
The symptoms of HUS include:
* Diarrhea
* Vomiting
* Abdominal pain
* Fatigue
* Weakness
* Shortness of breath
* Pale or yellowish skin
* Easy bruising or bleeding
If you suspect that someone has HUS, it is important to seek medical attention immediately. A healthcare provider will perform a physical examination and order blood tests to diagnose the condition. Treatment for HUS typically involves addressing the underlying cause of the condition, such as stopping certain medications or treating an infection. In some cases, hospitalization may be necessary to manage complications such as kidney failure.
Preventative measures to reduce the risk of developing HUS include:
* Practicing good hygiene, especially during outbreaks of diarrheal illnesses
* Avoiding certain medications that are known to increase the risk of HUS
* Maintaining a healthy diet and staying hydrated
* Managing any underlying medical conditions such as high blood pressure or diabetes.
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.
Here are some key points to define sepsis:
1. Inflammatory response: Sepsis is characterized by an excessive and uncontrolled inflammatory response to an infection. This can lead to tissue damage and organ dysfunction.
2. Systemic symptoms: Patients with sepsis often have systemic symptoms such as fever, chills, rapid heart rate, and confusion. They may also experience nausea, vomiting, and diarrhea.
3. Organ dysfunction: Sepsis can cause dysfunction in multiple organs, including the lungs, kidneys, liver, and heart. This can lead to organ failure and death if not treated promptly.
4. Infection source: Sepsis is usually caused by a bacterial infection, but it can also be caused by fungal or viral infections. The infection can be localized or widespread, and it can affect different parts of the body.
5. Severe sepsis: Severe sepsis is a more severe form of sepsis that is characterized by severe organ dysfunction and a higher risk of death. Patients with severe sepsis may require intensive care unit (ICU) admission and mechanical ventilation.
6. Septic shock: Septic shock is a life-threatening condition that occurs when there is severe circulatory dysfunction due to sepsis. It is characterized by hypotension, vasopressor use, and organ failure.
Early recognition and treatment of sepsis are critical to preventing serious complications and improving outcomes. The Sepsis-3 definition is widely used in clinical practice to diagnose sepsis and severe sepsis.
Reperfusion injury can cause inflammation, cell death, and impaired function in the affected tissue or organ. The severity of reperfusion injury can vary depending on the duration and severity of the initial ischemic event, as well as the promptness and effectiveness of treatment to restore blood flow.
Reperfusion injury can be a complicating factor in various medical conditions, including:
1. Myocardial infarction (heart attack): Reperfusion injury can occur when blood flow is restored to the heart muscle after a heart attack, leading to inflammation and cell death.
2. Stroke: Reperfusion injury can occur when blood flow is restored to the brain after an ischemic stroke, leading to inflammation and damage to brain tissue.
3. Organ transplantation: Reperfusion injury can occur when a transplanted organ is subjected to ischemia during harvesting or preservation, and then reperfused with blood.
4. Peripheral arterial disease: Reperfusion injury can occur when blood flow is restored to a previously occluded peripheral artery, leading to inflammation and damage to the affected tissue.
Treatment of reperfusion injury often involves medications to reduce inflammation and oxidative stress, as well as supportive care to manage symptoms and prevent further complications. In some cases, experimental therapies such as stem cell transplantation or gene therapy may be used to promote tissue repair and regeneration.
Symptoms of anaphylaxis include:
1. Swelling of the face, lips, tongue, and throat
2. Difficulty breathing or swallowing
3. Abdominal cramps
4. Nausea and vomiting
5. Rapid heartbeat
6. Feeling of impending doom or loss of consciousness
Anaphylaxis is diagnosed based on a combination of symptoms, medical history, and physical examination. Treatment for anaphylaxis typically involves administering epinephrine (adrenaline) via an auto-injector, such as an EpiPen or Auvi-Q. Additional treatments may include antihistamines, corticosteroids, and oxygen therapy.
Prevention of anaphylaxis involves avoiding known allergens and being prepared to treat a reaction if it occurs. If you have a history of anaphylaxis, it is important to carry an EpiPen or other emergency medication with you at all times. Wearing a medical alert bracelet or necklace can also help to notify others of your allergy and the need for emergency treatment.
In severe cases, anaphylaxis can lead to unconsciousness, seizures, and even death. Prompt treatment is essential to prevent these complications and ensure a full recovery.
Shock refers to a severe and sudden drop in blood pressure, which can lead to inadequate perfusion of vital organs such as the brain, heart, and lungs. There are several types of shock, including hypovolemic shock (caused by bleeding or dehydration), septic shock (caused by an overwhelming bacterial infection), and cardiogenic shock (caused by a heart attack or other cardiac condition).
Septic refers to the presence of bacteria or other microorganisms in the bloodstream, which can cause a range of symptoms including fever, chills, and confusion. Sepsis is a serious and potentially life-threatening condition that can lead to organ failure and death if left untreated.
Septic shock is a specific type of shock that occurs as a result of sepsis, which is the body's systemic inflammatory response to an infection. Septic shock is characterized by severe vasopressor (a medication used to increase blood pressure) and hypotension (low blood pressure), and it can lead to multiple organ failure and death if not treated promptly and effectively.
In summary, shock refers to a drop in blood pressure, while septic refers to the presence of bacteria or other microorganisms in the bloodstream. Septic shock is a specific type of shock that occurs as a result of sepsis, and it can be a life-threatening condition if not treated promptly and effectively.
Complement control protein
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Significance of Complement Regulatory Protein Tetraspanins in the Male Reproductive System and Fertilization. | Curr Protein...
Granzyme B: a new crossroad of complement and apoptosis
Complement Blood Test: MedlinePlus Medical Test
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Complement Deficiencies: Background, Pathophysiology, Epidemiology
Three studies point to same risk gene for age-related macular degeneration | National Eye Institute
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C‑reactive protein and cardiovascular disease: From animal studies to the clinic (Review)
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FY 2019 Congressional Justification | NIAMS
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Protein phosphatase 2A and complement component 4 are linked to the protective effect of APOE ɛ2 for Alzheimer's disease -...
Preclinical potential | Drug Discovery News
CD46 ELISA Kits
NIAAA Director's Report on Institute Activities to the 157th Meeting of the National Advisory Council on Alcohol Abuse and...
Decay accelerating activity of complement receptor type 1 (CD35). Two active sites are required for dissociating C5 convertases...
Inflammation11
- The new research, which was funded in part by the National Institutes of Health, solidifies a link between AMD and genes encoding the complement system, a set of proteins that plays a central part in immune responses and inflammation. (nih.gov)
- at the same time, the inflammation promoted by complement activation can result in cellular damage when not kept in check. (medscape.com)
- which is a group of immune system proteins that work together to destroy pathogens, trigger inflammation, and remove debris from cells and tissues. (nih.gov)
- Complement activation leads to the inflammation of the optic nerve and spinal cord that is characteristic of neuromyelitis optica, resulting in the signs and symptoms of the condition. (nih.gov)
- CRP is a highly sensitive marker of inflammation and tissue damage, and it is considered an acute phase protein ( 8 ). (spandidos-publications.com)
- Toward this goal, this initiative strongly encourages scientific collaborations among investigators with interest in cardiovascular, pulmonary or blood systems with investigators who study inflammation and immunology. (nih.gov)
- The C1 esterase inhibitor protein is required to control the 'complement' and 'contact' systems, collections of proteins in the blood that fight against infection and cause inflammation. (europa.eu)
- Inflammation and pus are both side-effects of the immune system doing its job. (howstuffworks.com)
- As noted on a supplement page from Davidson College's website , "the complement system consists of a series of plasma protein interactions which mediate direct attack on pathogens and induce inflammation … C5 plays a significant role in vital immunological pathways as well as contributing to several human diseases. (drugdiscoverynews.com)
- The production of antibodies against CNS proteins by infiltrating peripheral immune cells leads to autoimmune neurological disorders such as myasthenia gravis (MG). Inflammation resulting from damage to the BBB and infiltration of peripheral T-cells is also a pathogenic feature of multiple sclerosis (MS) and causes demyelination. (tocris.com)
- More detailed analyses revealed that the gene for complement component 1q (C1q), an important and evolutionarily ancient protein of the immune system, was expressed mainly by a subgroup of microglia responsible for driving inflammation, suggesting that it may contribute to lesion progression. (nih.gov)
Activation8
- Thus, tissue trauma is associated with early activation of both, the complement and apoptosis system. (nih.gov)
- Furthermore, dapsone and clofazimine could reduce rat-serum-mediated rabbit erythrocyte haemolysis in the presence of Mg2+-EGTA, indicating that they could also affect the alternative pathway of complement activation. (nih.gov)
- Serum glycoproteins participating in the host defense mechanism of COMPLEMENT ACTIVATION that creates the COMPLEMENT MEMBRANE ATTACK COMPLEX . (nih.gov)
- When CRP aggregates or binds to macromolecule ligands, the classical pathway of complement activation can be achieved through interactions with C1q ( 11 , 12 ). (spandidos-publications.com)
- Their studies explore how the complement system becomes activated by nanoparticles-and how to create new designs that could serve to prevent that activation and the adverse results that can occur in patients' bodies. (nih.gov)
- When they returned antibodies to the blood products, complement activation occurred as before or even stronger. (nih.gov)
- In all of the nanoparticles that we tested, complement activation was dependent on the binding of certain of these natural antibodies to nanoparticles," Simberg said. (nih.gov)
- If a person has a high level of antibodies that can recognize a particular type of nanoparticle, this person will have a high complement activation. (nih.gov)
Classical pathway2
- The classical pathway is triggered by interaction of the Fc portion of an antibody (immunoglobulin [Ig] M, IgG1, IgG2, IgG3) or C-reactive protein with C1q. (medscape.com)
- Lectins activate the lectin pathway in a manner similar to the antibody interaction with complement in the classical pathway. (medscape.com)
Pathways3
- In response to severe tissue trauma, several "molecular danger" sensing and signaling pathways are activated, especially the complement and the apoptosis cascade. (nih.gov)
- The complement cascade consists of 3 separate pathways that converge in a final common pathway. (medscape.com)
- Complement pathways and deficiencies. (medscape.com)
MEMBRANE ATTACK2
- C5a has an imperative role in chemotaxis and C5b forms the 1st part of the complement membrane attack complex. (prospecbio.com)
- The C5b macromolecular cleavage product forms a complex with the C6 complement component, and this complex is the basis for creation of the membrane attack complex, which includes supplementary complement components. (prospecbio.com)
Antibodies8
- This may be beneficial by leading to the clearance of unwanted material and dying cells in healthy brain development, but also pathogenic in the induction of neuronal cell death and production of antibodies against CNS proteins. (tocris.com)
- Among the corona proteins are natural antibodies that are part of each person's unique immunologic makeup. (nih.gov)
- Simberg's study found that these natural antibodies lead some people to mount an immune system attack on the nanoparticles prepared to treat their conditions. (nih.gov)
- The team observed that natural antibodies, called immunoglobulins, were among other proteins that formed on the nanoparticle corona. (nih.gov)
- Interestingly, the antibodies bind to the proteins in the corona, rather than to the pristine nanoparticle surface itself. (nih.gov)
- The team had published previously that that a nanoparticle's corona is important for complement attack, but this is the first study that pinpoints natural antibodies as the critical player in triggering immune attacks. (nih.gov)
- In another recent study, reported as a pre-print in bioRxiv, Veesler's team mapped dozens of distinct human antibodies capable of neutralizing SARS-CoV-2 by their ability to hit viral targets outside of the well-known spike protein [4]. (nih.gov)
- Such discoveries may form the basis for new and promising combinations of antibodies to treat COVID-19 that won't be disabled by concerning new variations in the SARS-CoV-2 spike protein. (nih.gov)
Genes3
- 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)
- Conestat alfa is produced by 'recombinant DNA technology': it is extracted from the milk of rabbits that have been given genes that make them able to produce the human protein in their milk. (europa.eu)
- For example, the present knowledge of genes controlling proliferation and migration of primordial germ cells (PGCs), precursors of gametes, is restricted in Atlantic halibut to embryonic expression of askopos ( kop ) and Tudor domain-containing protein 5 ( tdrd5 ) [ 19 ]. (biomedcentral.com)
Serum4
- Dapsone, clofazimine and rifampicin, the three most important constituents of multidrug therapy against leprosy, were studied with respect to their effects on the rat serum complement system, in vitro as well as in vivo. (nih.gov)
- ALN-CC5 engendered an up to 98.7-percent knockdown of serum C5 and an up to 96.8-percent inhibition of complement activity in non-human primates (NHPs) when administered subcutaneously on a weekly basis. (drugdiscoverynews.com)
- I am very encouraged by these preclinical data showing potent and durable knockdown of serum C5 with robust inhibition of complement activity using a subcutaneously administered RNAi therapeutic. (drugdiscoverynews.com)
- The encoded protein has cofactor activity for inactivation of complement components C3b and C4b by serum factor I, which protects the host cell from damage by complement. (antikoerper-online.de)
Pathway of complement1
- However, the latter pathway of complement consumption by these drugs seems to be insignificant because the factor-B-mediated complement-consumption system is minimal in rat sera. (nih.gov)
Gene3
- The protein encoded by this gene is a type I membrane protein and is a regulatory part of the complement system. (antikoerper-online.de)
- Finally, the protein encoded by this gene may be involved in the fusion of the spermatozoa with the oocyte during fertilization. (antikoerper-online.de)
- Complement Component C5a (C5a) is involved in the complement system and it is encoded by the C5 gene in human. (prospecbio.com)
Inhibition3
- This variant affects a part of the C3 protein that enables it to respond to inhibition by CFH. (nih.gov)
- These new preclinical data with our recently selected development candidate for ALN-CC5 demonstrate potent C5 knockdown and robust inhibition of complement activity in NHPs with weekly subcutaneous dosing. (drugdiscoverynews.com)
- We believe that these are promising results, since an over 80-percent inhibition of complement activity has been shown to be associated with clinical benefit. (drugdiscoverynews.com)
Receptor type3
- We show here that complement is critical for the induction of experimental autoimmune myocarditis and that it acts through complement receptor type 1 (CR1) and type 2 (CR2). (nih.gov)
- Decay accelerating activity of complement receptor type 1 (CD35). (wustl.edu)
- Dive into the research topics of 'Decay accelerating activity of complement receptor type 1 (CD35). (wustl.edu)
Pathogens2
- 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)
- The innate immunity and the complement system consist of 11 plasma proteins produced by the liver, usually activated by pathogens and antibody complexes, which help to eliminate pathogens. (listlabs.com)
Diseases9
- Complement and infectious diseases / author, Douglas P. Fine. (who.int)
- 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)
- [ 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)
- In many different diseases, the cause is actually an immune system error. (howstuffworks.com)
- Defects in one or more components of the immune system also cause increased susceptibility for autoimmune diseases and an increased risk of cancer. (cdc.gov)
- The compound is currently being developed for the treatment of complement-mediated diseases. (drugdiscoverynews.com)
- Complement component C5, which is largely expressed in liver cells, is a genetically and clinically validated target, and intravenous anti-C5 monoclonal antibody therapy has shown clinical activity and tolerability in several complement-mediated diseases. (drugdiscoverynews.com)
- Dysregulation of the complement system can lead to serious complications in a wide range of human diseases, including paroxysmal nocturnal hemoglobinuria, atypical hemolytic uremic syndrome and neuromyelitis optica," said Dr. Anita Hill, consultant hematologist for Leeds Teaching Hospitals NHS Trust in the United Kingdom and honorary senior lecturer at the University of Leeds . (drugdiscoverynews.com)
- If these results can be extended to the clinical setting, I believe that they could represent an attractive therapeutic strategy and potential new treatment option for patients with complement-mediated diseases. (drugdiscoverynews.com)
Bacteria3
- This system is made up of a group of proteins that work with the immune system to identify and fight disease-causing substances like viruses and bacteria. (medlineplus.gov)
- When activated, these proteins can essentially punch holes into bacteria and destroy them. (nih.gov)
- With his NIBIB grant, Simberg studies the complement system-an aspect of the immune system that originates from birth and is programmed to switch on when confronted by harmful viruses and bacteria. (nih.gov)
Underlying molecular1
- Although possible crossroads between both systems have been proposed, little is known about the underlying molecular interactions. (nih.gov)
Autoimmune disease6
- If the test shows that your complement protein levels are not normal or that the proteins aren't working with the immune system as well as they should, it can be a sign of an autoimmune disease or other serious health problem. (medlineplus.gov)
- If you are being treated for lupus or another autoimmune disease, increased amounts or activity of complement proteins may mean your treatment is working. (medlineplus.gov)
- These findings provide a mechanism by which activated complement, a key product of the innate immune response, modulates the induction of an autoimmune disease. (nih.gov)
- Specific complement deficiencies are also associated with an increased risk of developing autoimmune disease, such as SLE. (medscape.com)
- For example, recently completed population-based studies of lupus, an autoimmune disease where the body's immune system attacks healthy tissues, confirmed that women have a higher incidence of lupus than do men. (nih.gov)
- Multiple sclerosis (MS) is an autoimmune disease that is characterized by focal demyelination and axon degeneration in the central nervous system. (tocris.com)
Host defense1
- Cases of complement deficiency have helped defined the role of complement in host defense. (medscape.com)
Extracellular1
- To that end, truncated derivatives of CR1 whose extracellular part is composed of 30 tandem repeating modules, termed complement control protein repeats (CCPs), were generated. (wustl.edu)
20231
- Curr Protein Pept Sci;24(3): 240-246, 2023. (bvsalud.org)
Consists1
- The system consists of nine complement component proteins, called C1, C2, C3, and so on up to C9. (nih.gov)
Intricate3
- An intricate system regulates complement activity. (medscape.com)
- Both the innate and adaptive levels of the immune response involve secreted proteins, receptor-mediated signaling, and intricate cell-to-cell communication. (lumenlearning.com)
- The immune system is complex, intricate and interesting. (howstuffworks.com)
Humans1
- Beyond what is already known about bats' intriguing qualities, Veesler says humans still have much to discover about these flying mammals, including how their immune systems cope with such an onslaught of viral invaders. (nih.gov)
Binds2
- Approximately 70 percent of people with this disorder produce an immune protein called an antibody that attaches (binds) to the aquaporin-4 protein. (nih.gov)
- First, the immunoglobulin binds to the protein that is part of the corona of a nanoparticle (blue), followed by binding of C3 to the antibody. (nih.gov)
Natural Kille1
- 1 ) The genetic defects may affect one or more components of the immune system, including T cells, B cells, phagocytic cells, natural killer cells, and complement proteins. (cdc.gov)
Body's3
- Complement factors H and I (CFH and CFI) are proteins that inhibit the complement system and keep it from attacking the body's own cells. (nih.gov)
- Autoimmune disorders occur when the immune system malfunctions and attacks the body's own tissues and organs. (nih.gov)
- The primary function of the liver, kidneys, and urinary system is to expel toxins that result from the body's metabolism of food and drink 7 . (listlabs.com)
Microglia1
- Microglia act as 'scavengers' in the CNS, removing damaged/apoptotic cells and protein plaques and tangles, through phagocytosis mediated by the complement system. (tocris.com)
Vitro3
- In this study a new interaction interface is presented for C3a and C5a generation by the pro-apoptotic factor granzyme B. In vitro incubation of the central human complement components C3 and C5 with the serine protease granzyme B resulted in a concentration-dependent production of the anaphylatoxins C3a and C5a. (nih.gov)
- Of the three drugs only dapsone and clofazimine exhibited significant in vitro anti-complement activity and only at a very high, non-therapeutic dose of 0.24 mg/ml. (nih.gov)
- On the contrary, rifampicin could not induce significant in vitro complement consumption. (nih.gov)
Repeats2
- 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)
- 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)
Tissues2
- The aquaporin-4 protein is found in several body systems but is most abundant in tissues of the central nervous system. (nih.gov)
- The intent of this Request for Applications (RFA) is to stimulate research that will increase fundamental knowledge of the cellular and molecular components and mechanisms and signaling processes that regulate the immune system in cardiovascular, pulmonary, and blood tissues and are important in healthy tissue maintenance, damaged tissue repair, or disease pathogenesis. (nih.gov)
Cellular1
- While this mechanism might seemingly imply that host protein incorporation is a passive uptake of all cellular antigens associated with the plasma membrane at the site of budding, this is not the case. (mdpi.com)
Activity9
- A complement blood test measures the amount or activity of complement proteins in the blood. (medlineplus.gov)
- A CH50 test (sometimes called CH100) measures the amount and activity of all the major complement proteins. (medlineplus.gov)
- In a separate experiment we attempted to reconstitute the haemolytic complement activity consumed by dapsone and clofazimine by adding Crat-EDTA sera (a source of C3, C5, C6, C7, C8 and C9), but at most only 12% reconstitution of haemolytic activity could be achieved. (nih.gov)
- Deficiencies in complement predispose patients to infection via 2 mechanisms: (1) ineffective opsonization and (2) defects in lytic activity (defects in MAC). (medscape.com)
- Patients with low levels of this protein have excessive activity of these two systems, which leads to the symptoms of angioedema. (europa.eu)
- Further, comparative studies in a mouse arthritis model showed ALN-CC5 to be as effective as an anti-C5 antibody in reducing disease activity, demonstrating a necessary and sufficient role for liver-expressed C5 in localized complement-mediated disease," Dr. Akshay Vaishnaw, executive vice president and chief medical officer of Alnylam, commented in a news release. (drugdiscoverynews.com)
- Based on these results, we generated proteins one-fourth the size of CR1 but with enhanced decay accelerating activity for the C3 convertases. (wustl.edu)
- An NIH-funded team at the University of Colorado (UC) has assembled a clearer picture of the molecular activity that occurs when nanoparticles injected into the body are marked for immune system attack. (nih.gov)
- The kinetics of the hypoferraemic response and changes in levels of alternative complement activity in diploid and triploid Atlantic salmon, following injection of lipopolysaccharide. (elsevier.com)
Interaction1
- The present data suggest a new form of interaction between the complement and the apoptosis system on the level of granzyme B that is capable to generate C3a and C5a independently of the established complement proteases. (nih.gov)
Component4
- Immunoelectrophoretic study of mixtures of fresh rat sera and anti-leprosy drugs against specific anti-rat-C3 antisera demonstrated that dapsone and clofazimine could not cleave the C3 complement component. (nih.gov)
- CAMBRIDGE, Mass.-RNAi therapeutics company Alnylam Pharmaceuticals Inc. has released preclinical results regarding its development candidate for ALN-CC5, a subcutaneously administered investigational RNAi therapeutic that targets complement component C5. (drugdiscoverynews.com)
- Complement C5 is the 5th component of complement, which plays a central role in inflammatory and cell killing processes. (prospecbio.com)
- This process involves the fi lament aggregating protein, filaggrin , a protein component of keratohyalin granules. (criticalcaremcqs.com)
Antibody1
- Representation of C3 molecules of complement immune system binding to antibody. (nih.gov)
Innate and adaptive3
- The immune system comprises both innate and adaptive immune responses. (lumenlearning.com)
- We have demonstrated maternal transfer of innate and adaptive immune system transcripts into Atlantic halibut embryos and their relation with future embryo developmental potential. (biomedcentral.com)
- However, both innate and adaptive immune system-relevant factors are maternally transferred into teleost oocytes and present during embryonic development, before hatching [ 10 ]. (biomedcentral.com)
Viruses1
- The incorporation of biologically active host proteins into HIV-1 is a well-established phenomenon, particularly due to the budding mechanism of viral egress in which viruses acquire their external lipid membrane directly from the host cell. (mdpi.com)
Combination1
- 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)
Inflammatory2
- The complement system is a large group of proteins that work together to trigger inflammatory and immune responses that defend our bodies against infection. (nih.gov)
- CRP is an acute phase protein, while CVD is an inflammatory condition. (spandidos-publications.com)
Molecules1
- Recent research has indicated that some immune system -related cell surface molecules (CD molecules from the tetraspanin superfamily) may have a role in fertilization . (bvsalud.org)
Blood8
- What is a complement blood test? (medlineplus.gov)
- Why do I need a complement blood test? (medlineplus.gov)
- You may need a complement blood test if you have symptoms of an autoimmune disorder, especially lupus. (medlineplus.gov)
- You don't need any special preparations for a complement blood test. (medlineplus.gov)
- Are there any risks to a complement blood test? (medlineplus.gov)
- PURPOSE The National Heart, Lung, and Blood Institute (NHLBI) invites research grant applications to conduct studies on the immunobiology of health and disease in the cardiovascular, pulmonary, OR blood systems. (nih.gov)
- This Request for Applications (RFA), "Immunobiology of Cardiovascular, Pulmonary, and Blood Systems in Health and Disease," is related to one or more of the priority areas. (nih.gov)
- By examining concentrations of complement proteins in blood and cerebrospinal fluid in the week after aSAH, and comparing this with the clinical data, we may be able to predict who is most at risk in future. (brainfoundation.org.au)
Human5
- The active substance in Ruconest, conestat alfa, is a copy of the C1 esterase inhibitor protein and works in the same way as the natural human protein. (europa.eu)
- There are also all kinds of human ailments that are caused by the immune system working in unexpected or incorrect ways that cause problems. (howstuffworks.com)
- In addition, the encoded protein can act as a receptor for the Edmonston strain of measles virus, human herpesvirus-6, and type IV pili of pathogenic Neisseria. (antikoerper-online.de)
- Human Complement C5a produced in Human plasma having a molecular mass of 10.4 kDa. (prospecbio.com)
- In fact, his lab at the University of Washington, Seattle, was the first to elucidate the 3D architecture of the now infamous spike protein , which coronaviruses use to gain entry into human cells [1]. (nih.gov)
Deficiency2
- 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)
- These studies demonstrate that a Cys430-Phe mutation does not prevent the de novo synthesis of the b subunit, but alters the conformation of the mutant protein sufficiently to impair its intracellular transport, resulting in its deficiency in this patient. (embl.de)
Sepsis1
- Deficiencies in the complement cascade can lead to overwhelming infection and sepsis. (medscape.com)
Cascade1
- 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)
Components2
- We thus conclude that both dapsone and clofazimine could affect the complement system, predominantly through the earlier complement components and at very high, non-therapeutic doses. (nih.gov)
- 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)
Reactive3
- C‑reactive protein (CRP) and cardiovascular disease (CVD) have long been important research topics. (spandidos-publications.com)
- C-reactive protein (CRP) is an acute phase reactive protein. (spandidos-publications.com)
- This protein inhibits the accumulation of reactive oxygen species (ROS). (wikipedia.org)
Protective1
- In MS, the immune system attacks myelin, a protective layer that forms around nerve cells in the brain and spinal cord, leading to vision loss, muscle weakness, problems with balance and coordination, fatigue, numbness, and other debilitating symptoms. (nih.gov)
Cells1
- Some people have diabetes, which is caused by the immune system inappropriately attacking cells in the pancreas and destroying them. (howstuffworks.com)
Role4
- Contribution of the innate immune system to autoimmune myocarditis: a role for complement. (nih.gov)
- Genetic studies to date have shown that the complement system plays an important role in AMD. (nih.gov)
- The aquaporin-4 protein (AQP4), a normal protein in the body, plays a role in neuromyelitis optica. (nih.gov)
- The complement system evolved as part of the innate immune system and plays a key role in host defenses. (drugdiscoverynews.com)
Important2
- The complement system plays an important part in defense against pyogenic organisms. (medscape.com)
- That sounds gross, but it does show you something very important about your immune system. (howstuffworks.com)
Control1
- Three-dimensional structure of a complement control protein module in solution. (embl.de)
Immune system often2
- For example, organ transplants are much harder than they should be because the immune system often rejects the transplanted organ. (howstuffworks.com)
- For nanomedicine to achieve the envisioned breakthroughs in disease treatment, scientists must learn why the immune system often responds inhospitably to these therapies. (nih.gov)
Mechanism1
- Inside your body there is an amazing protectio-n mechanism called the immune system . (howstuffworks.com)