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Exploratory analysis of C4B GCN (gene copy numbers)showed positive correlation with neuropil contraction in the cerebellum and superior temporal gyrus among YASZ while AOSZ showed neuropil contraction in the prefrontal and subcortical structures. Thus, C4A and C4B GCN are associated with neuropil contraction in regions often associated with schizophrenia, and may be neuromaturationally dependent.
Comparative analysis of C4 alone, C4-Tryp, and C4-MASP2 revealed the impact of Tryp on C4 was similar as MASP2.
The purpose of this study was to evaluate C4A and C4B in patients with congenital adrenal hyperplasia in relation to CYP21A2 genotype and psychiatric and autoimmune comorbidity. We determined the copy numbers of C4A and C4B in 145 patients with CAH .No association was found between C4 copy number and autoimmune disease.
Low C4 in systemic lupus erythematosus patients is due to consumption rather than deficient synthesis related to lower C4A & B gene copy numbers.
Persistent C4d staining on kidney transplant follow-up biopsies was associated with worse clinical outcomes in patients with antibody-mediated rejection.
for the first time, a complete overview of C4 in SLE from genetic variation to binding capacity using a novel test. As this test detects crossing over of Rodgers and Chido antigens, it will allow for more accurate measurement of C4 in future studies.
results suggest that the C4B gene number associates positively with inflammation in patients with PIBD. Multiple copies of the C4B gene may thus aggravate the IBD-associated dysbiosis through escalated complement reactivity towards the microbiota.
An elevated number of C4 genes was observed in Alzheimer's disease (AD) patients as compared with healthy controls. The presence of high C4A and C4B copy numbers in AD patients could explain the increased C4 protein expression observed in AD patients, thus highlighting a possible role for C4A and C4B copy number variations in the risk of developing AD.
Quantification of plasma C4d+ microvesicles provides information about presence of antibody-mediated rejection, its severity and response to treatment in transplant patients.
The structural basis for inhibition of the classical and lectin complement pathways by S. aureus extracellular adherence protein binding to C4b has been presented.
The aims of this study were to elucidate the copy number variations of C4A and C4B in relation to disease risk in systemic lupus erythematosus, and to compare the basis of race-specific C4A deficiency between East Asians and individuals of European descent
C4d is expressed in esophageal squamous cell carcinoma
C4A and C4B gene copy numbers are stronger risk factors for juvenile-onset than for adult-onset systemic lupus erythematosus
Data indicate Ig-like transcript 4 (ILT4) as a cellular receptor for complement split products (CSPs) complement component 4d (C4d).
Suggest a prominent prognostic value of C4d staining as a rejection marker in ABO compatible kidney transplantation.
Isolated C4d deposition and isolated interstitial inflammation appear to be benign lesions, but C4d deposition in association with interstitial inflammation in the biopsy is strongly associated with the development of chronic graft dysfunction.
The interaction between C4BP and Leptospira interrogans LcpA, LigA and LigB is sensitive to ionic strength and inhibited by heparin.
Elevated levels of the complement activation product C4d in bronchial fluids is associated with lung cancer.
C4d immunostaining was a significant predictor of coronary allograft vasculopathy and death but not subsequent episodes of cell-mediated rejection. There was also a trend toward increased graft failure.
C4d-negative acute antibody-mediated graft rejection resembles C4d-positive aAMR in terms of clinical and pathological features. C4d positivity has no influence on short-term outcome.
These data show that Borrelia burgdorferi OspC inhibits the classical and lectin complement pathways and competes with complement protein C2 for C4b binding.
C4 mediated synapse elimination during postnatal development
role in suppressing autoantibody production elicited by S. pneumoniae antigens
Data indicate complement C3 deposition on peanut extract (PE) was abolished in immunoglobulin- and C4-deficient sera.
a deficiency in C4b does not alter radiation-induced lung disease in the C57BL/6 mouse model
C3 and C4 bind to collagen and elastin in the vascular wall and have a potential role in vascular stiffness and atherosclerosis
C4 modulates interstitial inflammation in experimental glomerulonephritis.
Complement C4 provides an important protective role against the development of systemic lupus erythematosus.
identified the murine follicular dendritic cell marker, FDC-M2, as complement c4. FDC-M2 was detectable at sites of immune complex-mediated inflammatory disease
C4 normally helps prevent early stages of autoimmune disease and that C4 deficiency predisposes to abnormal regulation of autoreactive B cells.
Macrophages derived from bone marrow produce sufficient C4 protein to restore the humoral response to NP-KLH hapten in C4-deficient animals when administered along with thymus-dependent antigen.
effects of complement depletion and deficiencies of C4, C5, and complement receptors 1 and 2 on mouse survival after intravenous exposure to S aureus
We found that deletion of the C4 gene does not significantly change either the time of onset or the severity and tempo of myelin oligodendrocyte-induced EAE compared with controls with a fully intact complement system.
In comparison with C57BL/6 mice, MRL/1pr mice had depressed C4 levels as early as 3 weeks of age.
The increased mortality of C4(-/-) or Factor B(-/-) mice indicates that these two pathways of complement activation are required for survival in mousepox.
Increased transcription of the complement C4 gene in the Rag1(-/-) intestine.
This gene encodes the basic form of complement factor 4, part of the classical activation pathway. The protein is expressed as a single chain precursor which is proteolytically cleaved into a trimer of alpha, beta, and gamma chains prior to secretion. The trimer provides a surface for interaction between the antigen-antibody complex and other complement components. The alpha chain may be cleaved to release C4 anaphylatoxin, a mediator of local inflammation. Deficiency of this protein is associated with systemic lupus erythematosus. This gene localizes to the major histocompatibility complex (MHC) class III region on chromosome 6. Varying haplotypes of this gene cluster exist, such that individuals may have 1, 2, or 3 copies of this gene. In addition, this gene exists as a long form and a short form due to the presence or absence of a 6.4 kb endogenous HERV-K retrovirus in intron 9.
C3 and PZP-like alpha-2-macroglobulin domain-containing protein 3
, Chido form of C4
, basic complement C4
, complement C4-B
, complement C4B1a
, complement component 4A
, complement component 4B
, complement component 4B (Chido blood group)
, complement component 4 (within H-2S)
, complement component 4B (Childo blood group)
, complement C4-like protein
, complement component 4, gene 2