Complement Factor H
Complement Factor B
Complement C3b Inactivator Proteins
Complement Factor I
Complement Factor D
Complement System Proteins
Complement Pathway, Alternative
Optic Disk Drusen
Complement C3-C5 Convertases
Complement Membrane Attack Complex
Polymorphism, Single Nucleotide
Complement Pathway, Classical
Complement Inactivator Proteins
Complement Inactivating Agents
Retinal Pigment Epithelium
Complement Hemolytic Activity Assay
Genetic Predisposition to Disease
Complement Activating Enzymes
Receptors, Complement 3b
Chromosomes, Human, Pair 1
Complement C4b-Binding Protein
Complement C3 Convertase, Alternative Pathway
Molecular Sequence Data
Receptor, Anaphylatoxin C5a
Amino Acid Sequence
Surface Plasmon Resonance
Chromosomes, Human, Pair 10
Pigment Epithelium of Eye
Complement Pathway, Mannose-Binding Lectin
Complement C1 Inhibitor Protein
Amino Acid Substitution
Complement Fixation Tests
Blood Bactericidal Activity
Protein Structure, Tertiary
Enzyme-Linked Immunosorbent Assay
Receptors, Complement 3d
Asian Continental Ancestry Group
Protein H, an antiphagocytic surface protein in Streptococcus pyogenes. (1/741)Surface-associated M protein is a major virulence factor in Streptococcus pyogenes which confers bacterial resistance to phagocytosis. However, many S. pyogenes strains also express additional structurally related so-called M-like proteins. The strain studied here is of the clinically important M1 serotype and expresses two structurally related surface proteins, the M1 protein and protein H. Mutants were generated that expressed only one or none of these proteins at the bacterial surface. For survival in human blood either protein H or M1 protein was sufficient, whereas the double mutant was rapidly killed. The protein-binding properties of protein H, M1 protein, and the mutants suggest that bacterial binding of immunoglobulin G and factor H or factor H-like protein 1, which are regulatory proteins in the complement system, contribute to the antiphagocytic property. (+info)
Multicenter trial of the quantitative BTA TRAK assay in the detection of bladder cancer. (2/741)BACKGROUND: Human complement factor H-related protein (hCFHrp) is produced by several bladder cancer cell lines and may be useful as a cancer marker. The aim of this study was to compare urinary hCFHrp and cytology for the detection of bladder cancer found by cystoscopy in patients with suggestive signs, symptoms, or preliminary test results. METHODS: The BTA TRAK assay, a quantitative enzyme immunoassay for the bladder tumor-associated antigen in urine, was compared with exfoliative cytology in 220 patients (155 men, 65 women; mean age, 64.2 years) presenting with signs, symptoms, or preliminary diagnostic results suggestive of this disease. Cystoscopy was the standard of detection. RESULTS: In the 100 patients found to have bladder cancer, the overall sensitivities of the BTA TRAK assay (at a previously determined decision threshold of 14 kilounits/L) and cytology were 66% (66 of 100) and 33% (33 of 100), respectively (P <0.001). The BTA TRAK assay proved to be statistically more sensitive than cytology for tumor grades I and II and for stage Ta and T1 tumors. In contrast, the overall specificity of the BTA TRAK assay in the 120 patients without cystoscopically confirmed bladder cancer was 69% (83 of 120) and that of cytology was 99% (119 of 120; P <0.001). The specificity of the BTA TRAK assay was higher in patients without benign or malignant genitourinary disease other than bladder cancer (76%; n = 89) than in patients with these conditions. When the BTA TRAK assay and cytology were used together such that a positive result in either test was scored as positive and the results compared with those of the BTA TRAK assay alone, increases in overall sensitivity and equivalent specificity were observed. CONCLUSION: Because of its relatively high sensitivity, the BTA TRAK assay could complement cytology as an adjunct to cystoscopy in the diagnosis and follow-up of most patients with bladder cancer. (+info)
In vitro analysis of complement-dependent HIV-1 cell infection using a model system. (3/741)Previous studies based on the use of human serum as a source of C have provided evidence for the C-dependent enhancement of cell infection by HIV-1. The present study was undertaken to distinguish C from other serum factors and to identify the proteins and the mechanisms involved in C-dependent cell infection by HIV-1. The classical C activation pathway was reconstituted from the proteins C1q, C1r, C1s, C4, C2, C3, factor H, and factor I; each were purified to homogeneity. A mixture of these proteins at physiological concentrations was shown to reproduce the ability of normal human serum to enhance the infection of MT2 cells by HIV-1 at low doses of virus. This enhancing effect was abolished when heat-inactivated serum and C2- or C3-depleted serum were used, and was restored upon addition of the corresponding purified proteins. A mixture of two synthetic peptides corresponding to positions 10-15 and 90-97 of human C receptor type 2 (CD21) as well as soluble CD4 both inhibited the C-dependent infection process. These data provide unambiguous evidence that HIV-1 triggers a direct activation of the classical C pathway in vitro and thereby facilitates the infection of MT2 cells at low doses of virus. These findings are consistent with a mechanism involving increased interaction between the virus opsonized by C3b-derived fragment(s) and the CD21 cell receptors and subsequent virus entry through CD4 receptors. (+info)
Disruption of disulfide bonds is responsible for impaired secretion in human complement factor H deficiency. (4/741)Factor H, a secretory glycoprotein composed of 20 short consensus repeat modules, is an inhibitor of the complement system. Previous studies of inherited factor H deficiency revealed single amino acid substitutions at conserved cysteine residues, on one allele arginine for cysteine 518 (C518R) and on the other tyrosine for cysteine 941 (C941Y) (Ault, B. H., Schmidt, B. Z., Fowler, N. L., Kashtan, C. E., Ahmed, A. E., Vogt, B. A., and Colten, H. R. (1997) J. Biol. Chem. 272, 25168-25175). To ascertain if the phenotype, impaired secretion of factor H, is due to the C518R substitution or the C941Y substitution and to ascertain the mechanism by which secretion is impaired, we studied COS-1 and HepG2 cells transfected with wild type and several mutant factor H molecules. The results showed markedly impaired secretion of both C518R and C941Y factor H as well as that of factor H molecules bearing alanine or arginine substitutions at the Cys518-Cys546 disulfide bond (C518A, C546A, C546R, C518A-C546A). In each case, mutant factor H was retained in the endoplasmic reticulum and degraded relatively slowly as compared with most other mutant secretory and membrane proteins that are retained in the endoplasmic reticulum. These data indicate that impaired secretion of the naturally occurring C518R and C941Y mutant factor H proteins is due to disruption of framework-specific disulfide bonds in factor H short consensus repeat modules. (+info)
Hypocomplementemia discloses genetic predisposition to hemolytic uremic syndrome and thrombotic thrombocytopenic purpura: role of factor H abnormalities. Italian Registry of Familial and Recurrent Hemolytic Uremic Syndrome/Thrombotic Thrombocytopenic Purpura. (5/741)Familial hemolytic uremic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP) carry a very poor outcome and have been reported in association with decreased serum levels of the third complement component (C3). Uncontrolled consumption in the microcirculation, possibly related to genetically determined deficiency in factor H--a modulator of the alternative pathway of complement activation--may account for decreased C3 serum levels even during disease remission and may predispose to intravascular thrombosis. In a case-control study by multivariate analysis, we correlated putative predisposing conditions, including low C3 serum levels, with history of disease in 15 cases reporting one or more episodes of familial HUS and TTP, in 25 age- and gender-matched healthy controls and in 63 case-relatives and 56 control-relatives, respectively. The relationship between history of disease, low C3, and factor H abnormalities was investigated in all affected families and in 17 controls. Seventy-three percent of cases compared with 16% of controls (P < 0.001), and 24% of case-relatives compared with 5% of control-relatives (P = 0.005) had decreased C3 serum levels. At multivariate analysis, C3 serum level was the only parameter associated with the disease within affected families (P = 0.02) and in the overall study population (P = 0.01). Thus, subjects with decreased C3 serum levels had a relative risk of HUS or TTP of 16.56 (95% confidence interval [CI], 1.66 to 162.39) within families and of 27.77 (95% CI, 2.44 to 314.19) in the overall population, compared to subjects with normal serum levels. Factor H abnormalities were found in four of the cases, compared with three of the healthy family members (P = 0.02) and none of the controls (P = 0.04) and, within families, factor H abnormalities were correlated with C3 reduction (P < 0.05). Reduced C3 clusters in familial HUS and TTP is likely related to a genetically determined deficiency in factor H and may predispose to the disease. Its demonstration may help identify subjects at risk in affected families. (+info)
Familial relapsing haemolytic uraemic syndrome and complement factor H deficiency. (6/741)BACKGROUND: In a recent study of three families we have found that inherited haemolytic uraemic syndrome (HUS) maps to a region of chromosome 1q containing the gene for complement factor H. In one of these families and also in a case of sporadic D-HUS, we have identified mutations in the factor H gene. A further family with inherited HUS has therefore been investigated. METHODS: DNA extracted from the family members and DNA extracted from archival post-mortem material from a deceased family member, was studied. Review of renal biopsies and study of complement components was also undertaken. RESULTS: This family demonstrates an inherited deficiency of complement factor H. Non-diarrhoeal HUS has affected at least two family members with half normal levels of factor H. CONCLUSION: These findings represent further evidence of the association between factor H dysfunction and HUS. (+info)
Identification of human complement Factor H as a ligand for L-selectin. (7/741)The selectin family of adhesion molecules (E-, P- and L-selectins) is involved in leukocyte recruitment to sites of inflammation and tissue damage. Recently it has been shown that L-selectin is involved not only in leukocyte tethering and rolling, but also plays an important role in leukocyte activation. For example, glycosylation-dependent cell-adhesion molecule 1 (GlyCAM-1), a known ligand for L-selectin, has been shown to enhance beta2-integrin function. GlyCAM-1 is a secreted protein and is present in mouse serum at a concentration of approx. 1.5 microg/ml. There is no obvious GlyCAM-1 homologue in man and, to date, L-selectin ligand(s) from human serum have not been characterized. Therefore we have used L-selectin affinity chromatography, followed by ion-exchange chromatography, to isolate specific ligand(s) for L-selectin. Using this procedure, we have isolated three major glycoproteins of apparent molecular masses 170 kDa, 70kDa and 50 kDa. The 170 kDa protein band was digested with trypsin and peptides were analysed by delayed extraction matrix-assisted laser desorption ionization MS and protein database searching. The 170 kDa protein was identified as the human complement protein Factor H. Human Factor H, isolated by a different method, was shown to bind specifically to L-selectin in the presence of CaCl2, and binding was inhibited by anti-L-selectin antibodies, fucoidan and lipopolysaccharide. Only a part of the purified Factor H preparation bound to immobilized L-selectin. The interaction of Factor H with leukocyte L-selectin was shown to induce the secretion of tumour necrosis factor-alpha (TNF-alpha). Pretreatment of Factor H with sialidase reduced both the binding of L-selectin to Factor H and the Factor H-induced L-selectin-mediated TNF-alpha secretion by leukocytes. Taken together, these results demonstrate that a post-translationally modified form of human plasma Factor H is a potential physiological ligand for L-selectin. (+info)
Resistance to both complement activation and phagocytosis in type 3 pneumococci is mediated by the binding of complement regulatory protein factor H. (8/741)To study the role of surface-associated proteins in the virulence of Streptococcus pneumoniae, we used two serotype 3 strains, ATCC 6303 and WU2, and two PspA-negative mutants of WU2, an encapsulated one, JY1123 (Caps(+)/PspA(-)), and an unencapsulated one, DW3.8 (Caps(-)/PspA(-)). ATCC 6303 and WU2 were highly virulent in mice, while the virulence of JY1123 was slightly decreased (50% lethal doses [LD(50)s], 24, 6, and 147 CFU/mouse, respectively); DW3.8 was avirulent (LD(50), 2 x 10(8) CFU). In vitro, ATCC 6303, WU2, and JY1123 (Caps(+)/PspA(-)) strongly resisted complement activation and complement-dependent opsonophagocytosis, whereas DW3.8 (Caps(-)/PspA(-)) was easily phagocytized in fresh serum. Trypsin treatment of ATCC 6303, WU2, and JY1123 (Caps(+)/PspA(-)) resulted in enhanced complement activation and complement-dependent opsonophagocytosis. Trypsin had no deleterious effect on the polysaccharide capsule. In addition, trypsin pretreatment of ATCC 6303 strongly reduced virulence upon intraperitoneal challenge in mice. This indicated that surface proteins play a role in the resistance to complement activation and opsonophagocytosis and contribute to the virulence of type 3 pneumococci. In subsequent experiments, we could show that the modulation of complement activation was associated with surface components that bind complement regulator factor H; binding is trypsin sensitive and independent of prior complement activation. Immunoblotting of cell wall proteins of the virulent strain ATCC 6303 with anti-human factor H antibody revealed three factor H-binding proteins of 88, 150, and 196 kDa. Immunogold electron microscopy showed a close association of factor H-binding components with the outer surface of the cell wall. The role of these factor H-binding surface proteins in the virulence of pneumococci is interesting and warrants further investigation. (+info)
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 symptoms of HUS include:
* Abdominal pain
* 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.
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.
Optic disk drusen (ODD) is a condition that affects the optic nerve and can cause vision loss if left untreated. It is characterized by the accumulation of lipids or other substances on the surface of the optic disk, which is the area where the retinal nerve fibers converge and leave the eye.
The symptoms of ODD can vary in severity and may include:
1. Blurred vision
2. Distorted vision
3. Eye pain or discomfort
4. Sensitivity to light
5. Reduced peripheral vision
If you are experiencing any of these symptoms, it is important to seek medical attention as soon as possible. ODD can be diagnosed through a comprehensive eye exam, which may include imaging tests such as optical coherence tomography (OCT) or visual field testing.
While there is no cure for ODD, there are several treatment options available that can help manage the condition and slow down its progression. These may include:
1. Vitamin supplements: Vitamins A, C, and E, as well as other antioxidants, may help reduce inflammation and slow down the progression of ODD.
2. Anti-inflammatory medications: Corticosteroids or other anti-inflammatory drugs may be prescribed to reduce inflammation and swelling in the eye.
3. Photodynamic therapy: This involves the use of a light-sensitive medication and low-intensity laser therapy to reduce inflammation and slow down the progression of ODD.
4. Laser surgery: In severe cases of ODD, laser surgery may be necessary to remove the accumulated lipids or other substances on the surface of the optic disk.
It is important to note that while these treatments can help manage the condition, they may not completely restore vision that has already been lost. Therefore, early detection and treatment are crucial to preventing or slowing down the progression of ODD.
Retinal drusen appear as small, flat spots or patches in the retina and are usually yellow or orange in color. They are made up of lipids (fatty substances) and other waste products that have accumulated in the retina over time. The exact cause of retinal drusen is not known, but they are thought to be related to the natural aging process and the decline in the function of the retina over time.
Retinal drusen can be diagnosed with a comprehensive eye exam, which includes a visual acuity test, dilated eye exam, and imaging tests such as optical coherence tomography (OCT). There is no treatment for retinal drusen, but they can be monitored with regular eye exams to ensure that they are not progressing or causing any vision problems.
In some cases, retinal drusen may be a sign of a more serious underlying condition such as macular degeneration, which can cause vision loss if left untreated. It is important for individuals over the age of 50 to have regular comprehensive eye exams to detect any changes in the retina and to prevent vision loss.
In summary, retinal drusen are small deposits that accumulate in the retina and are a common age-related change. They do not cause vision problems on their own but can be an early warning sign of more serious eye diseases such as macular degeneration. Regular comprehensive eye exams can detect any changes in the retina and prevent vision loss.
CNV develops when the underlying choroidal layers experience changes that lead to the growth of new blood vessels, which can leak fluid and cause damage to the retina. This can result in vision distortion, loss of central vision, and even blindness if left untreated.
The formation of CNV is a complex process that involves various cellular and molecular mechanisms. It is thought to be triggered by factors such as oxidative stress, inflammation, and the presence of certain growth factors and proteins.
There are several clinical signs and symptoms associated with CNV, including:
1. Distortion of vision, including metamorphopsia (distorted vision of geometric shapes)
2. Blind spots or scotomas
3. Decreased central vision
4. Difficulty reading or performing other daily tasks
5. Reduced color perception
6. Sensitivity to light and glare
The diagnosis of CNV is typically made based on a comprehensive eye exam, including a visual acuity test, dilated eye exam, and imaging tests such as fluorescein angiography or optical coherence tomography (OCT).
There are several treatment options for CNV, including:
1. Anti-vascular endothelial growth factor (VEGF) injections: These medications work by blocking the growth of new blood vessels and can help improve vision and reduce the risk of further damage.
2. Photodynamic therapy: This involves the use of a light-sensitive medication and low-intensity laser therapy to damage and shrink the abnormal blood vessels.
3. Focal photocoagulation: This involves the use of a high-intensity laser to destroy the abnormal blood vessels in the central retina.
4. Vitrectomy: In severe cases, a vitrectomy may be performed to remove the vitreous gel and blood vessels that are causing the CNV.
It is important to note that these treatments do not cure CNV, but they can help improve vision and slow the progression of the disease. Regular follow-up appointments with an eye care professional are necessary to monitor the condition and adjust treatment as needed.
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 term "geographic" refers to the characteristic map-like pattern of atrophy that occurs in the retina, with areas of degeneration resembling geographical features such as rivers, lakes, and islands. The progression of GA is typically slower than that of neovascular AMD, but it can still lead to significant vision loss over time.
The exact cause of GA is not fully understood, but it is believed to be related to the aging process and the accumulation of waste material in the retina. Risk factors for developing GA include age, family history, and prior history of AMD. There is currently no cure for GA, but various treatments are being developed to slow its progression and manage symptoms. These may include vitamin supplements, anti-inflammatory medications, and photodynamic therapy. Regular eye exams are important for early detection and monitoring of GA to help preserve vision and quality of life.
The term "serum sickness" was first used in the late 19th century to describe this condition, which was often seen in people who had received serum (a type of blood product) containing antibodies against diseases such as diphtheria or tetanus. Today, the term is still used to describe similar reactions to other substances, including medications and vaccines.
Serum sickness can be mild or severe, and in rare cases, it can lead to serious complications such as kidney failure or inflammation of the heart. Treatment typically involves stopping the use of the offending substance and providing supportive care to manage symptoms. In severe cases, corticosteroids or other medications may be used to reduce inflammation.
While serum sickness is a relatively rare condition, it is important for healthcare providers to be aware of it as a potential complication of medication and vaccine use. This knowledge can help them recognize and manage the condition effectively, reducing the risk of serious complications and improving outcomes for patients.
Complement factor I
Complement factor B
List of OMIM disorder codes
Complement component 3
Complement component 4B
Complement control protein
Complement (group theory)
Atypical hemolytic uremic syndrome
Complement component 2
Women's oversized fashion in the United States since the 1920s
Binary angular measurement
Brilliant (diamond cut)
Follicular dendritic cells
Frank Lloyd Wright
Homelessness in New Zealand
Atlantis The Palm, Dubai
European Train Control System
Trimeric autotransporter adhesin
Croatian Health Insurance Fund
Joe Hewitt (RAAF officer)
Complement factor I deficiency: MedlinePlus Genetics
Browsing by Subject "Complement Factor B"
Frontiers | A Novel Homozygous In-Frame Deletion in Complement Factor 3 Underlies Early-Onset Autosomal Recessive Atypical...
NIH VideoCast - NEI Symposium: Age-Related Macular Degeneration (AMD) and Complement Factor H
Factor H related proteins modulate complement activation on kidney cells - PubMed
Ultra-rare complement factor 8 coding variants in families with age-related macular degeneration - PubMed
On Demand: How Human Factors Can Complement Engineering in Civil Litigation: Principles and Case Studies
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Complement factor D, Human, ELISA kit
Recombinant Rat Complement factor D(Cfd) - Cusabio
Factors affecting IgG4-mediated complement activation. | Front Immunol;14: 1087532, 2023. | MEDLINE | Biblioteca Virtual...
COMPLEMENT AND INFLAMMATORY FACTORS IN AD PATHOGENESIS | NIH
Human CFH(Complement Factor H) ELISA Kit - ELISA Strip
Mouse Complement Factor D/CFD Protein (CFD-MM201) - KACTUS
British Model Works To Remodel The Complement Trade - Factor How
Characterisation of a heparin binding domain in complement factor H - Immunology
Search results for: complement factor h | National Eye Institute (NEI) Media Library
Active immunization against complement factor C5a: a new therapeutic approach for Alzheimer's disease
Prevalence and Phenotype Associations of Complement Factor I Mutations in Geographic Atrophy. - Oxford Stem Cell Institute
Complement Deficiencies: Background, Pathophysiology, Epidemiology
ACIP Altered Immunocompetence Guidelines for Immunizations | CDC
IJERPH | Free Full-Text | Long Covid-19: Proposed Primary Care Clinical Guidelines for Diagnosis and Disease Management
Monkey Complement Elisa Kit - Argentine Bioethics Association
Hemolytic anemia in a 26-year-old woman with vomiting and fatigue | CMAJ
Table 2 - Shiga Toxin-Associated Hemolytic Uremic Syndrome in Adults, France, 2009-2017 - Volume 27, Number 7-July 2021 -...
Which medications in the drug class Ophthalmics, Complement Inhibitors are used in the treatment of Exudative (Wet) Age-Related...
- Clinical significance of complement deficiencies. (medlineplus.gov)
- 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)
- Complement pathways and deficiencies. (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)
- Complement factor deficiencies are absent, only zinc need routinely be given in alternating fashion. (aaan.org)
- These multicomponent enzymes assemble on the surface of alternative pathway of complement activators and are stabilized by properdin (P). The participation of the alternative pathway of complement has been implicated in the pathogenesis of a wide variety of human diseases. (hycultbiotech.com)
- Properdin can bind C3b and activate the alternative complement pathway and also stabilizes the C3bBb alternative pathway C3 convertase enzyme, thereby directing the deposition of C3 fragments to the cell surface and driving the amplification loop ( 17 - 19 ). (frontiersin.org)
- This gene provides instructions for making a protein called complement factor I. This protein helps regulate a part of the body's immune response known as the complement system . (medlineplus.gov)
- Mutations in the CFI gene that cause complement factor I deficiency result in abnormal, nonfunctional, or absent complement factor I. The lack (deficiency) of functional complement factor I protein allows uncontrolled activation of the complement system. (medlineplus.gov)
- The unregulated activity of the complement system decreases blood levels of another complement protein called C3, reducing the immune system's ability to fight infections. (medlineplus.gov)
- Furthermore, factor D plays a role in fatty tissue distinct from its role as a complement protein. (hycultbiotech.com)
- The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself. (cusabio.com)
- Recombinant Mouse Complement Factor D/CFD Protein is expressed from HEK293 with hFc tag at the C-terminal.It contains Ile26-Ser259. (kactusbio.com)
- Adipsin protein production was analyzed in primary cultured orbital fibroblasts under insulin growth factor (IGF)-1, CD40 ligand ( CD40L ) stimulation, and adipogenesis . (bvsalud.org)
- Factor Xa is inactivated by protein Z-dependent protease inhibitor (ZPI), a serine protease inhibitor (serpin). (bionity.com)
- The affinity of this protein for factor Xa is increased 1000-fold by the presence of protein Z , while it does not require protein Z for inactivation of factor XI . (bionity.com)
- Defects in protein Z lead to increased factor Xa activity and a propensity for thrombosis. (bionity.com)
- Other homologous domains occur in related receptors, including the very low-density lipoprotein receptor and the LDL receptor-related protein/alpha 2-macroglobulin receptor, and in proteins which are functionally unrelated, such as the C9 component of complement. (embl.de)
- Notably, these pentraxins may also recruit soluble complement regulators, such as factor H (FH) and C4b-binding protein (C4BP), which in turn limit excessive complement activation on the surface ( 11 - 14 ). (frontiersin.org)
- Complement factor I deficiency is a disorder that affects the immune system. (medlineplus.gov)
- Some people with complement factor I deficiency have a kidney disorder called glomerulonephritis with isolated C3 deposits. (medlineplus.gov)
- Complement factor I deficiency can also be associated with autoimmune disorders such as rheumatoid arthritis or systemic lupus erythematosus (SLE). (medlineplus.gov)
- Complement factor I deficiency is caused by mutations in the CFI gene. (medlineplus.gov)
- Baracho GV, Nudelman V, Isaac L. Molecular characterization of homozygous hereditary factor I deficiency. (medlineplus.gov)
- Grumach AS, Leitao MF, Arruk VG, Kirschfink M, Condino-Neto A. Recurrent infections in partial complement factor I deficiency: evaluation of three generations of a Brazilian family. (medlineplus.gov)
- Ponce-Castro IM, Gonzalez-Rubio C, Delgado-Cervino EM, Abarrategui-Garrido C, Fontan G, Sanchez-Corral P, Lopez-Trascasa M. Molecular characterization of Complement Factor I deficiency in two Spanish families. (medlineplus.gov)
- The molecular basis of hereditary complement factor I deficiency. (medlineplus.gov)
- Cases of complement deficiency have helped defined the role of complement in host defense. (medscape.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)
- Inborn deficiency of factor X is very uncommon (1:500,000), and may present with epistaxis (nosebleeds), hemarthrosis (bleeding into joints) and gastrointestinal blood loss. (bionity.com)
- Apart from congenital deficiency, low factor X levels may occur occasionally in a number of disease states. (bionity.com)
- Deficiency of vitamin K or antagonism by warfarin (or similar medication) leads to the production of an inactive factor X. In warfarin therapy, this is desirable to prevent thrombosis . (bionity.com)
- American and British scientists described deficiency of factor X independently in 1953 and 1956, respectively. (bionity.com)
- 1997). "Inherited factor X deficiency: molecular genetics and pathophysiology. (bionity.com)
- Complement factor I and several related proteins protect healthy cells by preventing activation of the complement system when it is not needed. (medlineplus.gov)
- The interaction of the proteins C3, factor B, and factor D results in the formation of the alternative C3- and C5-convertases, i.e. (hycultbiotech.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)
- The FH-related (FHR) proteins share common ligands with FH, due to their homology with this complement regulator, but they lack the domains that mediate the complement inhibitory activity of FH. (frontiersin.org)
- Samples and standards are incubated in microtiter wells coated with antibodies recognizing human complement factor D. Biotinylated tracer antibody will bind to the captured human complement factor D. Streptavidin-peroxidase conjugate will bind to the biotinylated tracer antibody. (hycultbiotech.com)
- Description: This is Double-antibody Sandwich Enzyme-linked immunosorbent assay for detection of Human Complement Factor H (CFH) in serum, plasma and other biological fluids. (elisastrip.com)
- Lectins activate the lectin pathway in a manner similar to the antibody interaction with complement in the classical pathway. (medscape.com)
- Human IgG antibody Laboratories manufactures the monkey complement elisa kit reagents distributed by Genprice. (aabioetica.org)
- InflaRx N.V. is testing IFX-1, a monoclonal anti-human complement factor C5a antibody currently under development as treatment for inflammatory conditions and COVID-19 pneumonia. (who.int)
- Because of its significance as an threat to both human and related ungulates, such as cow, its genome was sequenced and still being studied to gain more insight into the virulence factor and to develop treatments and preventive prophylactic antibodies. (kenyon.edu)
- The human complement factor D ELISA kit is to be used for the in vitro quantitative determination of human complement factor D in serum, plasma and urine samples. (hycultbiotech.com)
- Description: A sandwich quantitative ELISA assay kit for detection of Mouse Complement Factor H (CFH) in samples from serum, plasma or other biological fluids. (elisastrip.com)
- The Monkey Complement Elisa Kit reagent is RUO (Research Use Only) to test human serum or cell culture lab samples. (aabioetica.org)
- Description: A sandwich ELISA for quantitative measurement of Monkey Complement Factor D in samples from blood, plasma, serum, cell culture supernatant and other biological fluids. (aabioetica.org)
- Description: A sandwich ELISA for quantitative measurement of Monkey Complement Factor H in samples from blood, plasma, serum, cell culture supernatant and other biological fluids. (aabioetica.org)
- Interactions of the FHRs with pentraxins resulted in enhanced activation of both the classical and the alternative complement pathways on dead cells when exposed to human serum. (frontiersin.org)
- The effects of settled grain dust on the human serum complement cascade were investigated. (cdc.gov)
- Some new clinical entities are linked with partial complement defects. (medscape.com)
- The alternative pathway of complement represents an important humoral component of natural defense against microbial attack. (hycultbiotech.com)
- The complement system is a key humoral component of innate immunity, and in addition to its many other functions, it is involved in the clearance of waste material, such as immune complexes and apoptotic and necrotic cells ( 1 , 2 ). (frontiersin.org)
- The human complement factor D ELISA is a ready-to-use solid-phase enzyme-linked immunosorbent assay based on the sandwich principle with a working time of 3½ hours. (hycultbiotech.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)
- The complement cascade consists of 3 separate pathways that converge in a final common pathway. (medscape.com)
- Dying cells also expose ligands that bind initiator molecules of the various complement pathways, so that complement activation and opsonin deposition on the dead cell surface may enhance phagocytotic clearance ( 1 , 8 ). (frontiersin.org)
- Factor H (FH), a major soluble complement inhibitor, binds to dead cells and inhibits excessive complement activation on their surface, preventing lysis, and the release of intracellular material, including DNA. (frontiersin.org)
- Mutations of complement factor I and potential mechanisms of neuroinflammation in acute hemorrhagic leukoencephalitis. (upmc.edu)
- The human factor X gene is located on the thirteenth chromosome (13q34). (bionity.com)
- Examples of high molecular environmental factors are known to influence the development weight occupational allergens include proteases used in the and expression of asthma, and a vast array of triggers of asthma detergent industry, laboratory animal allergens, and ovalbumin have been identified. (cdc.gov)
- Measurable quantities of factor D were detected in urine of 85% of healthy individuals (0.62 ± 0.33 ng/ml). (hycultbiotech.com)
- In vitro activation of the alternative pathway of complement by settled grain dust. (cdc.gov)
- 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)
- Factor X , also known by the eponym Stuart-Prower factor or as thrombokinase , is an enzyme ( EC 220.127.116.11) of the coagulation cascade . (bionity.com)
- The complement system plays an important part in defense against pyogenic organisms. (medscape.com)
- Because their roles in complement regulation is controversial and incompletely understood, we studied the interaction of FHR-1 and FHR-5 with DNA and dead cells and investigated whether they influence the regulatory role of FH and the complement activation on DNA and dead cells. (frontiersin.org)
- Factor D, a 24 kD serine protease of the alternative complement pathway, is synthesized as a precursor single-chain molecule. (hycultbiotech.com)
- Factor D is unique among serine proteases because it requires neither enzymatic cleavage for expression of proteolytic activity nor activation by a serpin for its control. (hycultbiotech.com)
- Bb, a serine protease, is generated when factor B is cleaved by COMPLEMENT FACTOR D into Ba and Bb. (bvsalud.org)
- Following these repeats is a 350 residue domain that resembles part of the epidermal growth factor (EGF) precursor. (embl.de)
- While HIV infection reports complement other HIV/AIDS studies of HIV infection in a community (5,6), AIDS surveillance and the HIV family of surveys (7) remain the basis for determining the current status and course of HIV infection in the United States. (cdc.gov)
- This difference in outcome may indicate that both donor and recipient factors contribute to the development of posttransplant TMA. (hindawi.com)
- An intricate system regulates complement activity. (medscape.com)
- Complement plays an essential role in the opsonophagocytic clearance of apoptotic/necrotic cells. (frontiersin.org)
- So that suspect case of Ebola disease or suspect case of Ebola disease definition is a person with signs and symptoms compatible with Ebola disease and an epidemiological risk factor within 21 days before the onset of symptoms. (cdc.gov)
- environmental factors that can increase agents and of primary interventions the risk of cancer. (who.int)
- Testing and reporting may be influenced by factors other than the incidence and prevalence of AIDS, e.g., public awareness of risk factors, confidentiality concerns, and testing accessibility. (cdc.gov)
- In healthy individuals factor D is rapidly eliminated via the kidney and neither modified extrarenal catabolism nor changes in synthesis contribute to elevated factor D levels observed in patients with renal failure. (hycultbiotech.com)
- Factor X is synthesized in the liver and requires vitamin K for its synthesis. (bionity.com)
- The human complement factor D concentration of samples, which are run concurrently with the standards, can be determined from the standard curve. (hycultbiotech.com)
- 1991). "Cloning and expression in COS-1 cells of a full-length cDNA encoding human coagulation factor X.". Gene 99 (2): 291-4. (bionity.com)
- The regenerative medicine is the combination of cells, material engineering, and biochemical factors to improve or replace the biological functions attempting to promote the medicine advancement. (bvsalud.org)