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PubMed1989

Size polymorphism of the erythrocyte complement receptor type 1 (CR1) in systemic lupus erythematosus induced by hydralazine.

The human erythrocyte complement receptor type 1 (CR1) is polymorphic with respect to molecular weight. Size variants with molecular weights of 190,000 (type A), 220,000 (type B) and 160,000 (type C) daltons have been detected in normal individuals (22 individuals), patients with hydralazine (Hz) lupus (n = 27), a group of Hz controls (n = 30) and the relatives of both Hz groups (27 and 11 individuals, respectively). The method of detection was SDS-polyacrylamide gel electrophoresis of erythrocyte membranes on low-percentage cross-linked gels followed by Western blotting using polyclonal rabbit anti-CR1 antibodies. In normal individuals, 77% had the A allotype and 26% carried the B allotype; amongst Hz lupus patients 67% carried the A allotype, 31% carried the B allotype, and 3% (1 individual) had the C allotype. Amongst the patients who had been on Hz but did not develop SLE, 83% carried the A allotype and 17% carried the B allotype. The AA phenotype was only found in 44% of Hz SLE patients but in 64% of normals and 70% of the Hz control group. Although not statistically significant, the results indicate a relative underrepresentation of the AA phenotype in patients with Hz-induced SLE. In addition, an equal or greater relative amount of the C allotype was detected in an Hz SLE patient with the AC phenotype. This is in contrast to lower relative amounts of the C allotype found in normal individuals with this phenotype.

Erythrocyte Membrane↗
PubMed1996

Low expression of erythrocyte complement receptor type 1 in chronic hepatitis C patients.

Primate erythrocyte complement receptor type 1 (CR1) plays an essential role in complement-associated immune complex clearance by transporting complexes to macrophages in the liver and/or spleen. Antibody-bound hepatitis C virus, which consists of immune complexes, is observed in patients with chronic hepatitis C. The aim of this study was to clarify the pathophysiological roles of erythrocyte CR1 in hepatitis C virus-infected individuals. We quantified the expression of erythrocyte CR1 with a fluorescence-activated cell sorter system in 57 chronic hepatitis C and 37 chronic hepatitis B cases and 20 normal volunteers. Complement-bound immune complexes were quantified by means of an enzyme-linked immunosorbent assay using anti-C1q and anti-C3d antibodies. Hepatitis C virus-infected patients showed lower erythrocyte CR1 and higher C3d immune complex levels than volunteers (P < 0.01 and P < 0.05, respectively). An inverse correlation was observed between the erythrocyte CR1 and C3d immune complex levels in hepatitis C virus infection (r = -0.300, P = 0.032). The erythrocyte CR1 levels in hepatitis C virus infection were lower in patients with severe liver inflammation, cirrhosis, or hepatocellular carcinoma than in those with mild inflammation, whereas the levels did not differ regardless of the disease stage in hepatitis B virus infection. These findings demonstrate that the expression of erythrocyte CR1 is related to immune complex quantity and the severity of liver disease in hepatitis C virus infection.

Adult↗
PubMed1989

Human T lymphocytes expressing the C3b/C4b complement receptor type one (CR1, CD35) belong to Fc gamma receptor-positive CD4-positive T cells.

The phenotypic characteristics of human T lymphocytes expressing the C3b/C4b complement receptor type one (CR1, CD35) were investigated using dual-color surface immunofluorescence and cytofluorometric analysis of stained peripheral blood mononuclear cells (PBMC) from normal individuals. Two to ten percent of PBMC coexpressed CR1 and the CD5, CD2, or CD3 antigen. CR1 was detected on a subset of CD4+ T lymphocytes but not on CD8+ or on Leu-7+ lymphocytes. Costaining for CR1 and for the CD4 subpopulation markers anti-Leu-8, TQ1, OKT17, 2H4, and 4B4 indicated that CR1 on lymphocytes may be coexpressed with any of these phenotypic determinants. All CR1+ lymphocytes expressed Fc gamma receptors (Fc gamma Rs) as assessed by their ability to bind biotinylated dimeric human IgG. The expression of CR1 was increased in mixed lymphocyte reaction with kinetics similar to those of HLA-DR antigen expression. Coexpression of CR1 and Fc gamma R+ may provide a subset of CD4+ lymphocytes with an enhanced ability to bind and respond to C3-bearing complexes of IgG and antigen.

Animals↗
PubMed2005

Review: complement receptor 1 therapeutics for prevention of immune hemolysis.

The complement system plays a crucial role in fighting infections and is an important link between the innate and adaptive immune responses. However, inappropriate complement activation can cause tissue damage, and it underlies the pathology of many diseases. In the transfusion medicine setting, complement sensitization of RBCs can lead to both intravascular and extravascular destruction. Moreover, complement deficiencies are associated with autoimmune disorders, including autoimmune hemolytic anemia (AIHA). Complement receptor 1 (CR1) is a large single-pass glycoprotein that is expressed on a variety of cell types in blood, including RBCs and immune cells. Among its multiple functions is its ability to inhibit complement activation. Furthermore, gene knockout studies in mice implicate a role for CR1 (along with the alternatively spliced gene product CR2) in prevention of autoimmunity. This review discusses the possibility that the CR1 protein may be manipulated to prevent and treat AIHA. In addition, it will be shown in an in vivo mouse model of transfusion reaction that recombinant soluble forms of CR1 can reduce complement-mediated RBC destruction, thereby prolonging survival of transfused RBCs. It is proposed that CR1-based therapeutics have potential for effective and safe prophylactic short-term use and for treatment of hemolytic transfusion reactions.

Anemia, Hemolytic, Autoimmune↗
PubMedDate not supplied

Inhibition of HIV-1 infection in vitro by monoclonal antibodies to the complement receptor type 3 (CR3): an accessory role for CR3 during virus entry?

Adhesion molecules are known to contribute to infectivity of HIV-1. Here we tested whether the complement receptor type 3 (CR3, CD11b), an alpha(m)beta2 integrin, plays an accessory role in the infection process of HIV-1, because ICAM-1, a ligand of CR3, is present on the envelope of HIV-1. In addition, the viral transmembrane protein gp41 shares four regions of homology with the complement component C3, a further CR3 ligand. Infection of PBMCs with HIV-IIIB and primary isolates was partially inhibited by anti-CR3 antibodies. A peptide derived from the complement component C3, covering the CR3-binding site of C3 and sharing strong similarity to the immunosuppressive region of gp41, significantly reduced the HIV-1 titer in infection assays. Recombinant soluble gp41 (rsgp41) and the peptide covering the immunosuppressive domain of gp41 inhibited the rosetting of iC3b-coated sheep erythrocytes with U937 via complement receptors (CRs) with an efficiency comparable to monoclonal anti-CR antibodies. In addition, sub-populations of CD4 + and CD8 + T-cells isolated from HIV-infected individuals were found to upregulate CR3 as determined by FACS analysis and on the mRNA level. Since gp41 has been implicated in viral fusion, an interaction of its C3-homology region in gp41 or an interaction of ICAM on the surface of free virus with CRs might contribute to facilitate viral entry.

Anti-HIV Agents↗
PubMed1976

Complement receptor lymphocytes in the rabbit I. an SIg-negative subpopulation in the appendix.

Complement receptor lymphocytes (CRL) were detected in various rabbit lymphoid tissues by the ability of these CRL to form rosettes with sheep red blood cells coated sequentially with rabbit antiserum directed against sheep red blood cell stroma and horse serum as a nonhemolytic source of complement (EAC). The rosette assay was shown to be specific for complement receptor (CR) activity and the EAC capable of detecting both C3b and C3d specific receptors. With lymphocyte preparations containing less than 5% phagocytic cells, the average per cent CRL in the various tissues studied was as follows: thymus 1%, popliteal lymph node 18%, spleen 30%, appendix 35%, and peripheral blood 45%. Double assays in which the lymphocytes were prestained with an FITC-labeled Fab fragment of a goat anti-rabbit Fab antibody before rosetting indicated that CRL were a subpopulation of surface immunoglobulin (SIg)-bearing lymphocytes in popliteal lymph node, spleen, and peripheral blood. In the appendix, however, in addition to finding SIg+ CR+ and SIg+ CR- populations, an SIg- CR+ population was consistently found. Double assays employing FITC-labeled goat antibodies specific for mu, alpha, and gamma determinants were also performed to determine if there was any relationship between the class of Ig displayed and presence of CR. It appeared that an approximately equivalent percentage of both IgM- and IgG-bearing cells also displayed CR. Experiments in which appendix cells were treated with Pronase to remove SIg and CR and the cells cultured in vitro to allow regeneration of surface markers confirmed the existence of SIg+CR+, SIg+CR-, and SIg-CR+ lymphocyte subpopulations. Whether the SIg-CR+, population represents a developing B cell population which will eventually also express SIg or whether it belongs to the T or "null" cell populations is unclear at present.

Animals↗
PubMed1992

Membrane expression and function of complement receptors CR1 and CR3 on neutrophils from HIV-infected subjects: modulation by rTNF-alpha and rGM-CSF.

We evaluated membrane expression and function of complement receptors CR1 and CR3 on neutrophils from 27 HIV-positive (HIV+) subjects (14 in the CDC class III and 13 class IV) as well as their modulation in vitro by recombinant tumour necrosis factor-alpha (rTNF-alpha) and granulocyte-macrophage colony stimulating factor (rGM-CSF). While CR1 was expressed at similar levels on neutrophils from controls and HIV+ subjects, CR3 expression was significantly higher in CDC class IV subjects than in healthy controls. CR1 and CR3 expression was significantly increased after treatment of neutrophils with both cytokines, without differences between controls and HIV+ subjects. Similarly, the superoxide anion (O2-) production in response to C3-coated zymosan (C3zy) was significantly enhanced on neutrophils from CDC class IV subjects when compared with controls. rGM-CSF and rTNF-alpha treatment significantly enhanced the spontaneous as well as C3zy-stimulated O2- production by neutrophils from controls and CDC class III subjects, and induced an upward trend in the CDC class IV group. These results indicate that the neutrophils of HIV+ patients are preactivated in vivo but they also indicate that these cells may correctly respond to a subsequent particulate stimulus as well as to activating cytokines. Our findings suggest that desensitization or functional exhaustion of complement receptors are not implicated in the abnormalities observed on neutrophils from HIV+ patients.

Adult↗
PubMed1993

Expression of complement receptor 2 (CR2) on HTLV-1-infected lymphocytes and transformed cell lines.

The expression of complement receptor 2 (CR2) has been demonstrated in established HTLV-1-transformed cell lines and in 12 studied de novo infected peripheral blood lymphocytes cultures, using 2 HTLV-1 sources. The simultaneous detection of CR2 and HTLV-1 antigens in both co-cultivated and supernatant-infected peripheral blood lymphocytes suggest that the increased CR2 expression is in tandem with the increasing HTLV-1 antigen expression. CR2 up-regulation seen during polyclonal activation is presumably in response to a viral protein, although a cellular factor has not been ruled out. Increasing CR2 expression during early infection suggests its possible involvement in selection or development of subsequent transformation events. Variable levels of CR2 in immortalized cell lines argue against its obligate expression of function in the maintenance of the transformed state. The expression of CR2 in cellular activation of T cells may be stage restricted. This study also expands the cellular distribution for CR2.

Cell Line↗
PubMed2005

A complement receptor-1 polymorphism with high frequency in malaria endemic regions of Asia but not Africa.

Complement receptor-1 (CR1) is a ligand for rosette formation, a phenomenon associated with cerebral malaria (CM). Binding is dependent on erythrocyte CR1 copy number. In Caucasians, low CR1 expressors have two linked mutations. We determined the Q981H and HindIII RFLP distribution in differing population groups to ascertain a possible role in adaptive evolution. We examined 194 Caucasians, 180 Choctaw Indians, 93 Chinese-Taiwanese, 304 Cambodians, 89 Papua New Guineans (PNG) and 366 Africans. PCR/RFLP used HindIII for CR1 expression and BstNI for the Q981H mutation. DNA sequencing and pyrosequencing were performed to resolve inconclusive results. Gene frequencies for the L allele were 0.15 in Africans, 0.16 in Choctaws, 0.18 in Caucasians, 0.29 in Chinese-Taiwanese, 0.47 in Cambodians and 0.58 in PNG. Allelic frequency for 981H were 0.07 in Africans, 0.15 in Caucasians, 0.18 in Choctaws, 0.29 in Chinese-Taiwanese, 0.47 in Cambodians and 0.54 in PNG. The Q981H polymorphism correlates with the HindIII RFLP in most groups except West Africans and appears to be part of a low CR1 expression haplotype. The gene frequency for the haplotype is highest in the malaria-endemic areas of Asia, suggesting that this haplotype may have evolved because it protects from rosetting and CM.

Africa↗
PubMed2001

No complement receptor 1 stumps on podocytes in human glomerulopathies.

BACKGROUND: Type one complement receptor (CR1) is the only physiological inhibitor of complement on podocytes. CR1 is lost in different glomerulopathies, in particular in lupus nephritis, in which it has been suggested that CR1 is removed by proteolysis from the cell membrane. METHODS: To define whether proteolytic cleavage of CR1 on podocytes is a general phenomenon, we analyzed the expression of CR1 in different glomerulopathies using a monoclonal antibody against epitopes present on the extracellular portion of the molecule and a polyclonal antibody directed at the intracellular tail of CR1. The two antibodies were applied on sequential serial histologic sections of renal biopsy. RESULTS: In normal glomeruli, the two antibodies provided similar results, that is, strong staining of podocytes, and both were shown to recognize specifically CR1. Decreased expression of the extracellular portion of CR1 was observed in lupus nephritis (8/8), focal and segmental glomerulosclerosis (FSGS; 7/7), IgA nephritis (6/6), membranous glomerulonephritis (3/3), and minimal change disease (3/3). In each case, the decreased expression was accompanied by a simultaneous decrease of the expression of the intracellular tail of CR1 (Spearman's correlation coefficient rs = 0.951, P < 0.001). This observation was confirmed by analyzing focal glomerular lesions on sequential serial sections. CONCLUSION: These data indicate that there are no CR1 stumps on podocytes, even in lupus nephritis, and suggest that the CR1 loss on podocytes is not due to consumption but to decreased synthesis. A loss of CR1 synthesis might render podocytes highly sensitive to complement attack.

Antibodies, Monoclonal↗
PubMed2006

Measurement of complement receptor 1 on neutrophils in bacterial and viral pneumonia.

BACKGROUND: A reliable prediction of the causative agent of community-acquired pneumonia (CAP) is not possible based on clinical features. Our aim was to test, whether the measurement of the expression of complement receptors or Fcgamma receptors on neutrophils and monocytes would be a useful preliminary test to differentiate between bacterial and viral pneumonia. METHODS: Sixty-eight patients with CAP were studied prospectively. Thirteen patients had pneumococcal pneumonia; 13 patients, influenza A pneumonia; 5 patients, atypical pneumonia, and 37 patients, aetiologically undefined pneumonia. Leukocyte receptor expression was measured within 2 days of hospital admission. RESULTS: The mean expression of complement receptor 1 (CR1) on neutrophils was significantly higher in the patients with pneumococcal pneumonia than in those with influenza A pneumonia. The mean expression of CR1 was also significantly higher in aetiologically undefined pneumonia than in influenza A pneumonia, but there was no difference between pneumococcal and undefined pneumonia. CONCLUSION: Our results suggest that the expression of CR1 is higher in classical bacterial pneumonia than in viral pneumonia. Determination of the expression of CR1 may be of value as an additional rapid tool in the aetiological diagnosis, bacterial or viral infection, of CAP. These results are preliminary and more research is needed to assess the utility of this new method in the diagnostics of pneumonia.

Adolescent↗
PubMed2000

Impact of TNFalpha, LTalpha, Fc gammaRII and complement receptor on HIV-1 trapping in lymphoid tissue from HIV-infected patients.

OBJECTIVES: To investigate HIV trapping mechanisms in patients with acute infection and in asymptomatic individuals prior to and during antiretroviral therapy. To determine the role of complement receptor (CR), Fc gamma receptor II (Fc gammaRII), tumour necrosis factor alpha (TNFalpha), and lymphotoxin alpha (LTalpha) expression in HIV trapping efficiency. METHODS: Lymphoid tissues from three acutely HIV-infected patients and six asymptomatic, chronically HIV-infected patients collected prior to and during antiretroviral therapy were compared with lymphoid tissues from six HIV-seronegative subjects. HIV, TNFalpha and LTalpha RNA expression was detected and quantified by fluorescence in situ hybridization. CR, Fc gammaRII and HIV p24 antigen were detected and quantified by fluorescence immunohistochemistry. RESULTS: The amount of trapped HIV did not differ significantly between patients with acute HIV infection and asymptomatic individuals, and was independent of the presence of CR or Fc gammaRII expression. However, in patients with acute infection, the amount of trapped virus was correlated inversely with the number of HIV-infected cells (P = 0.0092) and with the size of the light zone (P = 0.037). In these patients, the number of TNFalpha-expressing cells was correlated inversely with the amount of trapped virus (P = 0.014) and positively correlated with the size of the light zone in germinal centers (P = 0.041). No correlations were observed between TNFalpha or LTalpha expression and Fc gammaRII or CR expression. CONCLUSION: This report provides the first evidence that in humans TNFalpha is involved in the development of lymphoid follicles, HIV trapping, and, consequently, in early host immune responses. A model is proposed for early events in patients during acute HIV infection.

Acute Disease↗
PubMed1987

Cellular distribution of complement receptor type 4 (CR4): expression on human platelets.

Neutrophils have been shown to express a receptor for C3dg that is distinct from CR2 and is termed complement receptor type 4 (CR4). In the present study, other peripheral blood cell types were examined by indirect immunofluorescence and flow cytometry for the presence of C3dg binding activity. Specific uptake of C3dg occurred with neutrophils, platelets, and B lymphocytes, but not with eosinophils or T lymphocytes. Monocytes, contained within a mixed cell population of peripheral blood mononuclear cells and platelets, also bound C3dg, whereas purified monocytes did not. Binding of 125I-labeled glutaraldehyde-cross-linked C3dg to platelets was saturable, with an average of 1940 C3dg molecules bound per platelet at saturation (n = 8), ranging in number from 660 to 3930 molecules bound. Activation of platelets with thrombin did not consistently cause an increase in the expression of CR4 sites. 125I-C3dg binding to platelets was competitively inhibited equally well by unlabeled C3dg and iC3b, and approximately fourfold less well by C3b. The addition of platelets to elutriated monocytes generated C3dg binding activity on these cells by the formation of platelet-monocyte complexes. Thus, the CR4 on platelets accounted for the C3dg binding activity initially observed with partially purified monocytes. The adherent property of platelets may enable them to confer on certain other cell types the ability to localize C3dg-coated immune complexes or particles.

Blood Platelets↗
PubMed1985

Enhancement of human neutrophil complement receptors: a comparison of the rosette technique with the uptake of radio-labelled anti-CR1 monoclonal antibody.

We have compared the rosette technique (using C3b-coated red cells) with the uptake of a 125I F(ab')2 anti-complement receptor type 1 (CR1) monoclonal antibody (E11) for studying the phenomenon of chemotactic factor (fMLP)-induced complement receptor enhancement (CRE) on human neutrophils. With both methods the dose responses of fMLP were similar with maximal CRE being observed at 10(-7) moles 1(-1). Conversely, the time course of CRE and the effects of disodium cromoglycate (DSCG) on inhibition of enhancement were discrepant. Maximal CRE with the rosette method was observed at 30 min, whereas increased uptake of anti-CR1 had still not reached a plateau after 1 h. DSCG inhibited fMLP-induced CRE, as assessed by the rosette technique, whereas this agent had no effect on increased binding of radio-labelled anti-CR1 antibody. These results suggest that in CRE the increased adherence of C3b-coated red cells to fMLP-stimulated neutrophils, as measured by the rosette technique, is not dependent exclusively on the increased numbers of CR1.

Antibodies, Monoclonal↗
PubMed1994

Reduced expression of erythrocyte complement receptor (C3bR) in MS.

The study was carried out in patients with MS (n-121) and in control group (n-519). On the basis of haemagglutination intensity and results of radioimmunoassay three phenotypes of complement receptor were classified: high HH, medium HL, and low LL. Considerable differences were observed in the distribution of these phenotypes between controls and MS in whom the low phenotype was more frequent. Family studies suggest that reduced expression of the complement receptor on the erythrocytes depends in MS on the disease process in the first place, and not on genetic factors.

Erythrocytes↗
PubMed2002

Functional analysis of the human complement receptor 2 (CR2/CD21) promoter: characterization of basal transcriptional mechanisms.

Human complement receptor (CR) type 2 (CR2/CD21) is a 145-kDa membrane protein encoded within the regulators of complement activation gene cluster localized on human chromosome 1q32. Understanding the mechanisms that regulate CR2 expression is important because CR2 is expressed during specific stages of B cell development, and several lines of evidence suggest a role for altered CR2 function or expression in a number of autoimmune diseases. Additionally, even modest changes in CR2 expression are likely to affect relative B cell responses. In this study we have delineated the transcriptional requirements of the human CR2 gene. We have studied the human CR2 proximal promoter and identified sites important for controlling the level of transcription in CR2-expressing cells. We have determined that four functionally relevant sites lie within very close proximity to the transcriptional initiation site. These sites bind the transcription factors USF1, an AP-2-like transcription factor, and Sp1.

5' Untranslated Regions↗
PubMed1994

Soluble recombinant complement receptor 1 inhibits inflammation and demyelination in antibody-mediated demyelinating experimental allergic encephalomyelitis.

Activation of complement may contribute to tissue damage in many inflammatory diseases, including those that are clearly T cell driven. We have previously provided evidence that C is involved in tissue damage in multiple sclerosis and in the animal models of this disease, experimental allergic encephalomyelitis and Ab-mediated demyelinating experimental allergic encephalomyelitis, the latter being a model more closely resembling multiple sclerosis. The development of a soluble recombinant form of human complement receptor 1 (sCR1) with potent C-inhibiting activity both in vitro and in vivo provides a potential means of preventing C-mediated tissue damage in animal models and in human disease. Here, we describe the effects of this agent on clinical disease and pathology in Ab-mediated demyelinating experimental allergic encephalomyelitis in the rat. Daily i.p. injection of sCR1 (20 mg/kg) over 6 days completely suppressed serum C activity, reduced the severity of clinical disease (clinical score 1.33 vs 2.79 in untreated animals), inhibited central nervous system inflammation (inflammatory index 2.76 vs 6.55), and almost completely blocked demyelination (average 2.43% cord cross-section vs 8.81%). Deposition of C components C1, C3, and C9 was also markedly inhibited in sCR1-treated animals. This dramatic effect on a demyelinating disease, achieved using a well-tolerated biologic reagent, offers an exciting new prospect for therapy in multiple sclerosis.

Animals↗
PubMed2001

Structural studies in solution of the recombinant N-terminal pair of short consensus/complement repeat domains of complement receptor type 2 (CR2/CD21) and interactions with its ligand C3dg.

Human complement receptor type 2 (CR2, CD21) is a cell surface receptor that binds three distinct ligands (complement C3d, Epstein-Barr virus gp350/220, and the low-affinity IgE receptor CD23) via the N-terminal two of fifteen or sixteen short consensus/complement repeat (SCR) domains. Here, we report biophysical studies of the CR2 SCR 1-2 domain binding to its ligand C3dg. Two recombinant forms of CR2 containing the SCR 1-2 and SCR 1-15 domains were expressed in high yield in Pichia pastoris and baculovirus, respectively. Circular dichroism spectroscopy showed that CR2 SCR 1-2 receptor possessed a beta-sheet secondary structure with a melting temperature of 59 degrees C. Using surface plasmon resonance, kinetic parameters for the binding of either CR2 SCR 1-2 or the full-length SCR 1-15 form of CR2 showed that the affinity of binding to immobilized C3d is comparable for the SCR 1-15 compared to the SCR 1-2 form of CR2. Unexpectedly, both the association and dissociation rates for the SCR 1-15 form were slower than for the SCR 1-2 form. These data show that the SCR 1-2 domains account for the primary C3dg binding site of CR2 and that the additional SCR domains of full-length CR2 influence the ability of CR2 SCR 1-2 to interact with its ligand. Studies of the pH and ionic strength dependence of the interaction between SCR 1-2 and C3d by surface plasmon resonance showed that this is influenced by charged interactions, possibly involving the sole His residue in CR2 SCR 1-2. Sedimentation equilibrium studies of CR2 SCR 1-2 gave molecular weights of 17 000, in good agreement with its sequence-derived molecular weight to show that this was monomeric. Its sedimentation coefficient was determined to be 1.36 S. The complex with C3d gave molecular weights in 50 mM and 200 mM NaCl buffer that agreed closely with its sequence-derived molecular weight of 50 600 and showed that a 1:1 complex had been formed. Molecular graphics views of homology models for the separate CR2 SCR 1 and SCR 2 domains showed that both SCR domains exhibited a distribution of charged groups throughout its surface. The single His residue is located near a long eight-residue linker between the two SCR domains and may influence the linker conformation and the association of C3d and CR2 SCR 1-2 into their complex. Sedimentation modeling showed that the arrangement of the two SCR domains in CR2 SCR 1-2 is highly extended in solution.

Amino Acid Sequence↗