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PubMed1988

The rate of loss of CR1 from ageing erythrocytes in vivo in normal subjects and SLE patients: no correlation with structural or numerical polymorphisms.

The stability of CR1 (complement receptor type 1) on ageing erythrocytes in vivo was examined in a group of normal subjects who had been genotyped using a restriction fragment length polymorphism (detected using a cDNA probe for CR1) that correlates with the numerical expression of CR1 on normal erythrocytes (H = allele correlating with high expression, L = low). Erythrocytes were separated into 5 fractions of increasing age on discontinuous Percoll gradients. Mean CR1 numbers on erythrocytes fell from 636 molecules per cell in the first fraction to 384 in the fifth in the HH group and from 478 to 315 in the LL group. There was no difference in the rate of decline of CR1 numbers between the groups. A group of nine SLE patients was also studied in the same way; their genotypes were HH (four) and HL (five). Mean CR1 numbers amongst all of these patients fell from 477 to 232, a faster rate of decline than in a genotypically matched group of normal subjects. There was no difference in the prevalence of the different structural allotypes amongst 30 SLE patients compared with 21 normal subjects. These data provide further evidence that there are enhanced extracellular mechanisms for the removal of CR1 from erythrocytes of SLE patients and do not support the hypothesis that inherited variation in CR1 expression on erythrocytes increases disease susceptibility to SLE.

Cell Separation↗
PubMed1987

Abnormal podocyte CR-1 expression in glomerular diseases: association with glomerular cell proliferation and monocyte infiltration.

The expression of CR-1 complement receptors on glomerular epithelial cells, was studied in 77 renal biopsies from patients with (74) or without (3) glomerular diseases, employing an anti-CR-1 monoclonal antibody, and an indirect immunoperoxidase technique. Four patterns of CR-1 expression were recognised: normal (18); generally decreased (6); focal/segmental partial loss (44); and complete loss (9). Normal expression was detected in all three biopsies with non-glomerular diseases, and in glomerular diseases with normal glomeruli on light microscopy, but also in several glomerulonephritic biopsies (13), including diffuse proliferative lupus nephritis (1 of 7) and idiopathic membranous nephritis (5 of 14). However, the majority of biopsies from patients with glomerular diseases showed abnormal CR-1 expression (59 of 74), most evident in proliferative biopsies (43 of 49), with or without crescent formation (respectively, 18 of 20 and 25 of 29). Complete loss of CR-1 expression was almost restricted to crescentic biopsies (8 of 9). The abnormal CR-1 expression was unrelated to the presence of capillary immune deposits of Ig or C. More intraglomerular monocytes, assessed by monoclonal antibodies, were encountered in glomerulonephritic biopsies with partial CR-1 loss (median 6.2, P less than 0.05) or complete loss (median 14, P less than 0.03), than in biopsies with normal receptor expression (median 1.4). Thus, changes in glomerular CR-1 expression are frequently seen in many glomerular diseases and are associated with glomerular proliferative changes and monocyte infiltration, but not with the presence of capillary immune deposits.(ABSTRACT TRUNCATED AT 250 WORDS)

Antibodies, Monoclonal↗
PubMed1981

A murine B-cell lymphoma induced by Gross virus.

A B-lymphocyte tumor (MLB-MN line) was induced by Gross murine leukemia virus in Slc:ddY mice, successively passaged in normal adult mice, and adapted to tissue culture. The surface marker expression of MLB-MN was examined and found to include several markers that are known to occur in normal B-lymphocytes. The cells bore surface immunoglobulin M, detected by indirect immunofluorescence staining, and Fc receptors and complement receptors, detected by rosette formation. Thy 1 antigen and secretion of immunoglobulin were lacking. These results have led us to postulate that the origin of the MLB-MN tumor was a late differentiation stage of the B-lymphocyte.

AKR murine leukemia virus↗
PubMed1978

Identification of a receptor for complement on the guinea pig alveolar macrophage membrane.

The present study was undertaken in an attempt to demonstrate the presence of a receptor for complement on the membrane of guinea pig alveolar macrophages (PAM). When target cells were prepared using mouse serum as the complement source, no attachment or ingestion of the target cell by guinea pig PAM was observed. When fresh autologous guinea pig serum was used as the complement source, attachment and ingestion of the target cell by PAM were observed. The results of additional experiments demonstrated that the attachment of these target cells was mediated by a complement receptor. These results demonstrated that like human PAM, guinea pig PAM do possess a membrane receptor for complement.

Animals↗
PubMed2006

To be or not to be B7.

The activation of lymphocytes and development of adaptive immune responses is initiated by the engagement of TCRs by antigenic peptide-MHC complexes and shaped at the clonal level by both positive and negative costimulatory signals. The B7 family members are involved at several stages in this process. In this issue of the JCI, Vogt et al. show that the B7 family-related protein V-set and Ig domain-containing 4 (VSIG4) can act as an inhibitor of T cell activation (see the related article beginning on page 2817). Intriguingly, the same molecule was recently independently identified as a complement receptor of the Ig superfamily (CRIg) and was convincingly demonstrated to be a receptor for complement component 3 fragments. These findings raise interesting questions regarding the physiological roles and mechanisms of action of this molecule. Identification of dual functions of this molecule provides an additional level of complexity in T cell costimulation.

Animals↗
PubMed2001

Ontogeny of the follicular dendritic cell phenotype and function in the postnatal murine spleen.

Follicular dendritic cells (FDCs) represent a unique cell population of antigen trapping cells restricted to follicles within the secondary lymphoid tissues. FDCs appear to be involved in the formation of primary follicles during the ontogeny of lymphoid tissue. We sought to determine the kinetics and tissue distribution of cells in the spleen of newborn mice expressing various differentiation antigens restricted to FDCs using immunohistochemistry with monoclonal antibodies (mAb) against FDCs and in vivo immune complex binding and retention. The earliest FDC-specific marker displayed was the antigenic determinant recognized by the FDC-M1 mAb, which was detectable by Day 3 prior to follicle formation on cells located around the peripheral part of the developing white pulp. The appearance of CD21/35 (complement receptor Type 2 and 1, CR1.2) was observed at the end of the first week, revealing a focal pattern in B-cell-rich areas. In addition, at that time there were some FDC-M1-positive cells in the nonfollicular part of the periarteriolar region. The administration of anti-horseradish peroxidase antibody followed by soluble antigen HRP into 7-day-old newborn mice resulted in the trapping and retention of immune complexes onto FDCs even in the absence of Fcgamma receptors. The appearance of another FDC-specific marker, FDC-M2, was observed during the second week after birth and was restricted on the cells located in the same area as CR1.2 cells. The Fcgamma receptor Type II appeared on FDCs after the second postnatal week. The above sequence of phenotypic maturation could also be observed in newborns after lethal irradiation at Day 3. This indicates that not only mature FDCs but also their precursors are highly radioresistant, and their phenotypic maturation follows a programmed path that requires only a small number of mature B cells.

Animals↗
PubMed1984

Complement C3 receptors: structure and function.

Significant progress has been made during the past few years toward elucidating the structure and function of various C3 receptors. Better understanding of the biochemical basis of the immune adherence phenomenon has been achieved. The availability of polyclonal and monoclonal antibodies to C3 receptors allowed more accurate studies of the cellular distribution of these receptors. Finally, advances in our knowledge of the functional properties of the C3 receptors and their relationship to specific cell surface molecules was facilitated by recognition of a patient deficient in various receptor-mediated functions. All together these developments will soon make it possible to describe in detail the molecular events involved in the modulation of complement receptor coupled cell functions.

Animals↗
PubMed1978

Human peripheral lymphocytes bearing surface immunoglobulin do not have readily detectable Fc receptors.

The question of whether human peripheral B lymphocytes have Fc receptors was examined directly by double-label immunofluorescent techniques utilizing assays for detection of Fc receptors, surface immunoglobulin, and complement receptors. Fc receptors were detected by indirect immunofluorescence after incubation with soluble antigen-antibody complexes. Complement receptors were detected by the binding of fluoresceinated bacteria coated with complement. It was demonstrated that most surface immunoglobulin-bearing, complement-receptor positive lymphocytes did not bind soluble antigen-antibody complexes. Conversely, most cells which readily bound soluble complexes did not have surface immunoglobulin or complement receptors. Therefore, most peripheral B lymphocytes do not have easily detectable Fc receptors and most Fc receptor-bearing lymphocytes do not have B cell markers.

Antigen-Antibody Complex↗
PubMed1976

Two biochemical markers in lymphocyte subpopulations.

Human blood lymphocytes can be separated into two populations according to the presence of surface complement receptors. Lymphocytes containing complement receptors (CR+) were found to have a high rate of RNA synthesis or turnover accompanied by increased protein synthesis. Lymphocytes not containing complement receptors (CR-) while maintaining a low profile in RNA synthesis, had a 10-12-fold greater activity in adenosine deaminase enzyme which is believed to be related to lymphocyte-immune responses and cell-mediated immunity. These two biochemical characteristics can be useful tools for future studies in lymphocyte functions. By using these two biochemical markers, we found that CLL lymphocytes were predominantly of the CR+ type, had high active RNA synthesis, and very low adenosine deaminase level. Lymphocytes from two patients with X-linked agammaglobulinaemia showed a picture opposite to that of CLL.

Adenosine Deaminase↗
PubMed2002

Complement activation alters myocellular sodium homeostasis during polymicrobial sepsis.

OBJECTIVE: To determine whether complement activation alters sodium homeostasis in fast-twitch skeletal muscles during sepsis, and if protein kinase-C is involved in this process. DESIGN: Prospective, randomized, controlled animal study. SETTING: Research laboratory. SUBJECTS: Male Sprague-Dawley rats weighing 60-75 g. INTERVENTIONS: Rats underwent cecal ligation and puncture (CLP) or sham-operation with or without soluble complement receptor-1 treatment. Soluble complement receptor-1 (20 mg/kg) was administered intraperitoneally 5 mins before operation. Twenty-four hours after operation, fast-twitch extensor digitorum longus muscles were isolated and incubated in normal Krebs-Henseleit buffer (pH 7.4). In addition, extensor digitorum longus muscles isolated from normal rats were incubated for 1 hr in the Krebs-Henseleit buffer media containing normal rat sera, zymosan-activated (4 or 10 mg/mL) rat sera, or heat-inactivated rat sera. Ten percent diluted rat sera were used as a complement source in all groups. Last, extensor digitorum longus muscles isolated from normal rats were incubated for 1 hr in the Krebs-Henseleit buffer media containing zymosan-activated or heat-inactivated rat sera in the presence of protein kinase-C inhibitors (i.e., 4 microM GF109203X or 5 microM rottlerin). Soluble C5b-9 complex concentrations in zymosan-activated human sera were determined by enzyme-linked immunosorbent assay to evaluate the degree of complement activation induced by zymosan. MEASUREMENTS AND MAIN RESULTS: Incubated extensor digitorum longus muscles from CLP, sham-operated, or normal rats were used to measure intracellular Na+ and K+ contents ([Na+]i or [K+]i). Polymicrobial sepsis, as produced by CLP, markedly increased [Na+]i and [Na+]i/[K+]i ratios in fast-twitch extensor digitorum longus muscles 24 hrs after CLP compared with sham operation. Administration of soluble recombinant complement receptor 1 before operation significantly decreased myocellular [Na+]i and [Na+]i/[K+]i ratios. Zymosan profoundly elevated soluble C5b-9 concentrations in human sera in vitro. Sublytic zymosan-activated rat sera significantly increased myocellular [Na+]i and [Na+]i/[K+]i ratios relative to heat-inactivated rat sera. No difference in myocellular [Na+]i and [Na+]i/[K+]i ratios was observed when we used 4 mg/mL compared with 10 mg/mL of zymosan for activation. Last, incubation of extensor digitorum longus muscles with GF109203X or rottlerin significantly attenuated increases in myocellular [Na+]i and [Na+]i/[K+]i ratios induced by sublytic zymosan-activated rat sera. CONCLUSIONS: Polymicrobial sepsis alters sodium homeostasis in fast-twitch skeletal muscles, which is significantly attenuated by administration of soluble complement receptor 1. Protein kinase-C inhibition completely blocks changes in myocellular [Na+]i and [Na+]i/[K+]i ratios induced by sublytic zymosan-activated rat sera. Collectively, these results suggest that an inappropriate activation of complement is, at least in part, responsible for changes in skeletal muscle sodium homeostasis during sepsis, and activation of PKC is one of the intracellular signaling pathways by which complement activation alters myocellular sodium homeostasis.

Animals↗
PubMed2002

Structure-function studies of the receptors for complement C1q.

C1q is an essential component of the phylogenetically ancient innate complement (C) system and is crucial to our natural ability to ward off infection and clear toxic cell debris (e.g. amyloid fibrils, apoptotic cells). Several candidate C1q receptors [C1q receptor for phagocytosis enhancement (C1qRp), complement receptor (CR) 1, calreticulin (CRT), binding protein for the globular head of C1q (gC1qbp)] have been described, and the aim of this review is to shed light on their structure-function relationships. One cell-surface molecule, C1qRp, has emerged as a defence collagen receptor for C1q, as well as mannose-binding lectin (MBL) and surfactant protein A. C1qRp (also known as the AA4 antigen in rodents) is the antigen recognized by a pro-adhesive monoclonal antibody called mNI-11 and antibodies against CD93, but recent results failed to confirm C1q binding activity. CR1 (CD35), a multifunctional receptor both in its ligand specificity and in its C regulation activities, is found on circulating monocytes and neutrophils, but the major site of expression is B-lymphocytes. As a receptor, CR1 binds to C1q, other C opsonins (C4b, C3b, iC3b) and MBL, and as such, has been involved in promoting phagocytosis. Several studies support a role for the cell surface receptor for the collagenous domains of C1q (cC1qR; also known as CRT). CRT belongs to the family of heat-shock proteins, the most abundant and ubiquitous soluble intracellular proteins. Though CRT does not have a transmembrane domain, it seems to mediate phagocytosis of the apoptotic cells through association with CD91. A 33 kDa protein interacts with the globular head of C1q and, logically, has been termed gC1qbp. This protein is located in mitochondria, suggesting that gC1qbp is not a cell-surface receptor itself.

Animals↗
PubMed1978

Isolation of various canine leucocytes and their characterization by surface marker analysis.

Various techniques were used to separate canine peripheral blood leucocytes into populations enriched in lymphocytes, polymorphonuclear leucocytes, phagocytic mononuclear cells (monocytes) and macrophages. Surface markers on each cell population were determined by rosette formation. Fc receptors for IgG and complement receptors (C3b and C3d) were present on PMN, monocytes, macrophages as well as on a sub-population of lymphocytes. Purification of the lymphocytes into T-and B-cell-enriched populations revealed that these receptors were present only on the B lymphocytes and not on the T lymphocytes. In addition, a third lymphocyte population, which did not possess surface immunoglobulin, and Fc receptor but not the complement receptor. None of the cell populations exhibited C4 complement receptors or Fc receptors for IgM. When different cell populations were tested for their ability to form rosettes directly with human type 'O' red blood cells it was found that most populations could rosette, suggesting that this technique could not be used as a specific marker for canine T lymphocytes.

Animals↗
PubMed2004

Possible role of factor XIII subunit A in Fcgamma and complement receptor-mediated phagocytosis.

Besides its traditional role in hemostasis, factor XIII subunit A (FXIII-A) is supposed to function as a cellular transglutaminase and to be involved in certain intracellular processes, including cytoskeletal remodeling. To investigate its intracellular role, the aim of the present study was to follow changes in FXIII-A production in combination with the receptor-mediated phagocytic activities of monocytes/macrophages and to examine the phagocytic functions of monocytes in patients with FXIII-A deficiency. Human blood monocytes were isolated from the buffy coats of healthy volunteers and cultured for 4 days. The FcgammaR-mediated phagocytosis of sensitized erythrocytes (EA) and the complement receptor (CR)-mediated phagocytosis of complement-coated yeast particles were studied during monocyte/macrophage differentiation. Changes in the gene expression of FXIII-A were detected by real-time quantitative RT-PCR. FXIII-A protein production was investigated with fluorescent image analysis at single cell level and Western immunoblot analysis. Both the FcgammaR and CR-mediated phagocytosis increased during culturing, which peaked on day 3. The phagocytic activity of the cells could be markedly inhibited with monodansylcadaverine, an inhibitor of the transglutaminase-induced crosslinking of proteins. The phagocytosis of EA, complement-coated and uncoated yeast particles was found to be strongly diminished in monocytes of FXIII-A deficient patients. The phagocytic functions of cultured cells showed a change in parallel with the alterations in FXIII-A mRNA expression, as well as with that in FXIII-A in protein synthesis detected by image and Western immunoblot analyses in concert. Our results suggest that FXIII-A plays a role in the Fcgamma and complement receptor-mediated phagocytic activities of monocytes/macrophages.

Blotting, Western↗
PubMed1993

Antibody feedback regulation in MRL/lpr mice.

MRL/Mp-lpr/lpr (MRL/l) mice spontaneously develop autoimmune disease, characterized by glomerulonephritis, polyarteritis and polyarthritis. The lpr mice have defects in the Fas antigen, which plays a role in apoptosis, and it has been suggested that lack of negative selection of autoreactive T cells explains the initiation of the disease. The extremely high amount of autoantibodies may reflect additional immunoregulatory abnormalities. Antibody feedback regulation is an efficient way of up- or downregulating antibody responses. We have for the first time determined whether IgG-mediated suppression as well as IgM-mediated enhancement operates normally in these mice. MRL/l and MRL/Mp(-)+/+ (MRL/n) mice of different ages were therefore immunized with sheep erythrocyte (SRBC)-specific IgG or IgM antibodies followed by SRBC. Control groups received antigen alone. Five days later, the antigen-specific plaque-forming cell response was measured. IgG induced more than 90% suppression in both MRL/l and MRL/n in mice of all ages tested. This degree of suppression is in the same range as for other, normal mouse strains. In contrast, IgM-mediated enhancement was completely absent in 12-week-old MRL/l mice but normal in 8-week-old MRL/l as well as in MRL/n mice of all ages tested. When spleens and lymph nodes were immunohistochemically studied using a mAb specific for complement receptors 1 and 2 (CR1/CR2), an abnormal follicular structure was demonstrated in 12-week-old MRL/l mice. The antibody response of both 8- and 13-week-old MRL/l mice in vivo, after downregulation of these receptors, was inhibited by 85-96%. Thus, the presented data demonstrate that MRL/l mice with overt autoimmune disease are refractory to IgM-mediated enhancement of antigen-specific antibody production. We believe that this abnormal antibody feedback regulation is due to abnormal follicular structure in lymphoid organs of old MRL/l mice, hence the inability to localize and present antigen in a normal way.

Animals↗
PubMed2002

A role for the Cr2 gene in modifying autoantibody production in systemic lupus erythematosus.

Systemic lupus erythematosus is an autoimmune disease characterized by autoantibody production against nuclear Ags. Recent studies suggest that the Cr2 gene, which encodes for complement receptor (CR)1 and CR2, is important in disease susceptibility. Because the precise disease phenotype related to this gene, in isolation or in relation to other genetic loci, is not known, we analyzed C57BL/6 mice with a targeted mutation in Cr2 (C57BL/6.Cr2(-/-)) with or without a concomitant mutation in Fas (C57BL/6.lpr Cr2(-/-)). The Cr2(null) mutation in a C57BL/6.lpr background markedly increases the serum concentrations of IgG1 and IgG2b and the levels of antinuclear and anti-dsDNA Abs as compared with C57BL/6.lpr controls. There is also a trend for higher concentrations of IgG2a and IgG3. In contrast, isolated deficiencies in either these CRs or Fas have a limited effect in the production of anti-dsDNA Abs. Moreover, the Cr2(null) mutation does not affect other disease manifestations. These findings demonstrate that abnormalities in CR1 and CR2 may be linked to the production of autoantibodies by modifying the effect of other systemic lupus erythematosus susceptibility genes. Phenotypic expression of other disease manifestations need additional Cr2-independent genetic factors.

Animals↗
PubMed1993

A requirement for membrane-associated phospholipase A2 in platelet cytotoxicity activated by receptors for immunoglobulin G and complement.

Platelets are potent antibody- and complement-dependent cytotoxic effector cells. We showed previously that a single platelet can lyse a target cell sensitized with immunoglobulin G (IgG) and complement components up to C3 (C integral of 3b denotes the target cell-bound fragment of complement up to C3; the precise nature of the bound C3 fragment has not been established), and that the complete cytotoxic system capable of specific recognition and lysis resides in platelet membranes. To define the components of platelet membranes required for cytotoxicity, a set of inhibitors of phospholipase A2 (PLA2) that act by different chemical mechanisms was tested. The lytic reaction is blocked at appropriate concentrations of bromophenacylbromide, mepacrine, and manoalide. When platelets are treated with bromophenacylbromide, inhibition of cytolytic activity and that of PLA2 enzymatic activity occur in parallel. Platelets release arachidonate when incubated with target cells bearing IgG and C integral of 3b, confirming that Fc gamma R and complement receptor trigger both PLA2 action and efficient lysis. Inhibition by thimerosal of a reverse reaction, i.e., reacylation catalyzed by acyltransferase, causes increased target cell lysis, presumably by increasing the products of PLA2 action. Platelet cytotoxicity is increased when platelets are pretreated with some products of PLA2: exogenous lysophospholipids and not free arachidonic acid increase cytotoxicity. Electron microscopy suggests that platelets and target cells may fuse, possibly as a result of the formation of lysophospholipids which are well-known membrane fusogens. Fixation with paraformaldehyde does not affect platelet cytotoxicity, suggesting that the complete cytotoxic system resides as a preformed complex in platelet membranes. The results indicate that platelet membrane-associated PLA2, together with receptors for Fc and complement, are required for platelet cytotoxicity.

Animals↗