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PubMed1976

Membranoproliferative glomerulonephritis. Localization of early components of complement in glomerular deposits.

A body of evidence suggests that in membranoproliferative glomerulonephritis (MPGN), complement is activated by the alternate pathway. Therefore, deposition of early components of complement should not be expected in glomeruli. The renal tissues of 16 patients--13 with classic MPGN and 3 with dense deposit disease, a variant of MPGN--were studied by light and electron microscopy and by means of elution and immunofluorescence for the localization of complement (C1q, C4, and C3), immunoglobulins (1gG, IgM, and 1gA), and other serum proteins. Variable amounts of C3, C4 and/or C1q, and IgM were detected in the glomeruli of all patients, whereas IgG and IgA were present, respectively, in 15 of 16 and 6 of 16 patients. Deposits were localized in mesangium and in peripheral capillary loops in a typical lobular distribution. The specificity of each antiserum was verified by immunodiffusion, immunoelectrophoresis, and blocking experiments utilizing unlabeled antibody. Glomerular-bound IgG was eluted with acid citrate buffer, suggesting that IgG might be complexed with antigen(s) in glomerular deposits. By light microscopy, lesions ranged from focal proliferation and lobulation to more severe involvement with typical splitting of glomerular basement membranes, sclerosis, and less frequently, crescent formation. Ultrastructurally, all patients with classic MPGN exhibited mesangial and subendothelial deposits, and in 5 of these patients, subepithelial deposits were demonstrated. With the exception of ultrastructural lesions, patients with the dense deposit variant lacked distinguishable features when compared with those with classic MPGN. The significance of these findings is discussed in relation to a) activation of complement and the possible role of an immune complex mechanism and b) the variability of the morphologic expression.

Adolescent↗
PubMed2000

Adiponectin, a new member of the family of soluble defense collagens, negatively regulates the growth of myelomonocytic progenitors and the functions of macrophages.

We investigated the functions of adiponectin, an adipocyte-specific secretory protein and a new member of the family of soluble defense collagens, in hematopoiesis and immune responses. Adiponectin suppressed colony formation from colony-forming units (CFU)-granulocyte-macrophage, CFU-macrophage, and CFU-granulocyte, whereas it had no effect on that of burst-forming units-erythroid or mixed erythroid-myeloid CFU. In addition, adiponectin inhibited proliferation of 4 of 9 myeloid cell lines but did not suppress proliferation of erythroid or lymphoid cell lines except for one cell line. These results suggest that adiponectin predominantly inhibits proliferation of myelomonocytic lineage cells. At least one mechanism of the growth inhibition is induction of apoptosis because treatment of acute myelomonocytic leukemia lines with adiponectin induced the appearance of subdiploid peaks and oligonucleosomal DNA fragmentation. Aside from inhibiting growth of myelomonocytic progenitors, adiponectin suppressed mature macrophage functions. Treatment of cultured macrophages with adiponectin significantly inhibited their phagocytic activity and their lipopolysaccharide-induced production of tumor necrosis factor alpha. Suppression of phagocytosis by adiponectin is mediated by one of the complement C1q receptors, C1qRp, because this function was completely abrogated by the addition of an anti-C1qRp monoclonal antibody. These observations suggest that adiponectin is an important negative regulator in hematopoiesis and immune systems and raise the possibility that it may be involved in ending inflammatory responses through its inhibitory functions. (Blood. 2000;96:1723-1732)

Adiponectin↗
PubMed1978

[The influence of intraoperative autotransfusion (IAT) on plasmaproteins in patients with posttraumatic intraabdominal bleeding or hemorrhage during vascular surgery (author's transl)].

In 29 patients (12 vascular and 17 trauma cases) the effect of intraabdominal bleeding and surgical management under intraoperative autotransfusion on several plasmaproteins was examined. The following parameters were monitored immediately before and after autotransfusion as well as 24, 48, 72 hours and one week later, in the thawed serum: 1. albumen and the carrier proteins prealbumen, transferrin, retinol-binding protein, 2. acute phase reactants: c-reactive protein coeruloplasmin, haptoglobin, 3. fractions of complement: C1q, C3c, C5 and C 3-activator, 4. serum-cholinesterase. With usual treatment by infusion of electrolyte solutions during operation and the following days, and further applicated blood transfusion, plasma and fresh frozen plasma by clinical needs, while the immediate blood loss during operation was replaced by autotransfusion, there was no change in preoperative dates. Only at the 3rd day the typical picture of catabolic situation of the postoperative period was observed in vascular cases and not at all in trauma cases. Thus the changes were closely related to the preexisting disease or state of shock, without further detoriation by intraoperative autotransfusion. 7 days later a sometimes overshooting normalization of the parameters was observed. Only cholinesterase remained extremely low, especially in vascular cases.

Abdominal Injuries↗
PubMed2001

Endothelial cells, megakaryoblasts, platelets and alveolar epithelial cells express abundant levels of the mouse AA4 antigen, a C-type lectin-like receptor involved in homing activities and innate immune host defense.

Phagocytic complement C1q receptor (C1qRp) and thrombomodulin (TM, CD141), are two key members of a novel family of lectin receptors involved in cell-cell interactions and innate immune host defense. We report here that the mouse homologue of human C1qRp (AA4) and TM are derived from a common ancestor on the basis that both genes co-localized to the same region of the chromosome 2 and also because they share similar domain composition and organization. Moreover, we found that mouse AA4 was localized to sites known to express TM. Mouse AA4 was identified by Western blot as a heavily glycosylated protein (110 kDa) expressed in all tissues tested. Brain and spleen expressed an additional 130-kDa band. Immunoperoxidase and double-immunofluorescence experiments showed that, surprisingly, the major site of AA4 expression in all tissue tested is on endothelial cells and that despite the apparent involvement of AA4 in the phagocytic response, it is not expressed by tissue macrophages. In contrast, megakaryoblasts (in bone marrow and spleen) and platelets expressed abundant levels of AA4 stored in cytoplasmic vesicles. Interestingly, alveolar epithelial cells (lung) but not other epithelia (e.g. uterus) were strongly stained for AA4. Although AA4 has been described on all hematopoietic progenitors, we found that only circulating immature B cells, monocytes and NK cells but not T cells and neutrophils expressed AA4.

Amino Acid Sequence↗
PubMed1990

Trimer and tetramer complexes containing C1 esterase inhibitor, C1r and C1s, in serum and synovial fluid of patients with rheumatic disease.

During activation, the first component of complement C1q (C1r-C1s)2 is dissociated in conjunction with the formation of complexes containing C1 esterase inhibitor (C1-INH). Trimer complexes, with zymogen C1s associated with a firm C1-INH-C1r complex (C1-INH-C1r-C1s) can be distinguished from tetramer complexes C1-INH-C1r-C1s-C1-INH) in which C1-INH is firmly bound to both proteases. In the present study a two-stage electroimmunoassay was developed for the specific measurement of C1-INH-C1r-C1s. In the first step, C1-INH and its complexes were immunoprecipitated with anti-C1-INH during electrophoresis in the presence of Ca2+. In the second step, C1s contained in C1-INH-C1r-C1s was dissociated in the presence of EDTA and was measured by immunoprecipitation with anti-C1s. C1-INH-C1r-C1s were consistently found in normal sera. Normal sera did not contain C1-INH-C1r-C1s-C1-INH as assessed with a previously described ELISA procedure. Sera and synovial fluids from two groups of patients with inflammatory arthritis were investigated. In rheumatoid arthritis patients (n = 15) C1-INH-C1r-C1s complexes were usually found at high concentration both in serum and synovial fluid. C1-INH-C1r-C1s-C1-INH complexes were also present with values that were higher in synovial fluid than in serum, in accord with previous findings of classical pathway activation in the inflamed joints of the patients. Patients with spondylarthritic syndromes (n = 7) had serum and synovial fluid C1-INH-C1r-C1s concentrations that were comparable to those of the rheumatoid arthritis patients. If at all present, C1-INH-C1r-C1s-C1-INH were detected in trace amounts. Thus, C1 activation in patients with spondylarthritic syndromes appeared to be efficiently controlled at the C1r level. Distinguishing between C1-INH-C1r-C1s and C1-INH-C1r-C1s-C1-INH may prove of value in further studies of the activation and control of C1 in disease.

Animals↗
PubMed1986

Circulating immune complexes in Meniere's disease.

Sixty-six patients with Meniere's disease were studied for possible general immunologic abnormalities. The disease was bilateral in 20 cases, causing active symptoms in 49. Thirty-six healthy control subjects were also studied. Immune activity was assessed by quantitative measurement of the circulating immune complexes, serum immunoglobulin assay, and acetate electrophoresis, and by an autoantibody screen to a battery of ten general tissue antigens. Thirty-six (54.5%) of the 66 patients with Meniere's disease were found to have significantly raised circulating immune complex levels compared with one (2.9%) of the 36 controls. A statistically significant increased incidence of autoantibodies was also found in the Meniere's group.

Adolescent↗
PubMed1989

Solitary plasmacytoma of the skull revealed by a mononeuritis multiplex associated with immune complex vasculitis.

We describe a patient with solitary plasmacytoma of the skull, in whom mononeuritis multiplex was the presenting manifestation. Some features of the POEMS syndrome (plasma cell dyscrasia with polyneuropathy, organomegaly, endocrinopathy, monoclonal [M] protein, skin changes), including thrombocytosis, were found. Muscle and nerve biopsies disclosed a small vessel hypersensitivity-type vasculitis and complement-fixing immune complex deposits in vessel walls. Removal of the plasmacytoma resulted in clinical improvement and clearance of the vasculitis and immune complex deposits.

Adult↗
PubMed1992

Selective inhibition of immune complex trapping by follicular dendritic cells with monoclonal antibodies against rat C3.

The role of complement component C3 in the trapping of immune complexes by follicular dendritic cells (FDC) was studied in the rat, by means of the C3-specific monoclonal antibody ED11. Immunocytochemistry revealed the presence of C3 on FDC, where it co-localized with trapped peroxidase anti-peroxidase complexes. Furthermore, C3 was detected on reticular cells occupying the T cell areas of peripheral lymphoid organs, which are not involved in the handling of immune complexes. The in vivo administration of anti-C3 abolished the trapping of immune complexes in splenic follicles, but was unable to release preexisting complexes from the FDC. Trapping of immune complexes was also prevented by treatment of rats with cobra venom factor (CoVF). While CoVF caused massive depletion of C3 from serum, ED11 treatment had no such effect. The effect of anti-C3 appeared at least in part to be due to an inhibition of complement activation by immune complexes. We also analyzed earlier stages of the trapping process, with respect to their C3 dependence. Upon systemic injection immune complexes are initially observed in the marginal zone. Administration of anti-C3 reduced this localization, indicating a role for C3 in the entry of immune complexes into the spleen. Our results confirm experiments in CoVF-treated animals and extend the evidence for a role of C3 in the follicular trapping process using anti-C3 in vivo. The mechanism of immune complex trapping and the role of complement therein is discussed.

Animals↗
PubMed1982

Complement components in kidney allograft recipients: relationship to cytomegalovirus infection.

Serum complement profiles of 19 renal transplant recipients were studied serially before and after renal transplantation to determine if there is any relationship between cytomegalovirus (CMV) infection and alteration in the serum complement (C) levels. Most patients had low serum C3 and C4 levels before transplantation, but afterwards these levels increased in some patients. Clq was elevated before and after transplantation. Factor B was low before transplantation, but after surgery, its level approached normal in patients without cytomegalovirus viremia, whereas in those with viremia, Factor B level became even more depressed. Circulating Factor B fragments were found in the sera of five out of seven patients with active cytomegalovirus infection, which suggests activation of the alternative pathway possibly related to active CMV infection.

Adult↗
PubMed1996

Perforant path transection induces complement C9 deposition in hippocampus.

The presence of complement system proteins in amyloid plaques and the up-regulation of several complement mRNAs in neurons and glial cells in affected brain regions during Alzheimer disease (AD) provided a basis for further examination of complement protein expression in a rodent lesion model of AD. Perforant path transection in rats was used as a model for the degeneration of entorhinal cortex (EC) layer II neurons and the consequent deafferentation of the hippocampus that occurs during AD. Immunostaining for C9, a key terminal component of the complement cascade membrane attack complex (MAC), showed extracellular C9 deposition in parenchyma around the EC wound and in hippocampus as early as 1 day, and disappeared by 14 days postlesion. Apoptosis of EC layer II neurons was seen and was presumably due to severing of their axonal projections to the hippocampus by the transection lesion. However, apoptotic EC layer II neurons were not immunostained by anti-rat C9 antibody, suggesting complement was not involved in inducing apoptosis. In the deafferented hippocampus, extracellular C9 immunostaining was localized to the dentate gyrus middle molecular layer, a region of synaptic loss, dendritic degeneration, and early synaptogenesis. In addition, intracellular C9 immunostaining was seen only in select hippocampal interneurons. Dentate gyrus granule neurons and pyramidal neurons were not C9 immunostained. Clusterin (SGP-2), a soluble inhibitor of the MAC that is up-regulated in AD, was also detected in the wound area (extracellular), the dentate gyrus middle molecular layer (extracellular), and intracellularly in scattered hippocampal interneurons. The data support the hypothesis that the complement system generally participates in responses to brain injury, as well as in AD.

Afferent Pathways↗
PubMed1983

DNA antibodies and complement in SLE patients. A follow-up study.

Sixty-seven patients with systemic lupus erythematosus (SLE) were followed up for 3-19 months (mean 12) in a prospective study. The activity of SLE was estimated on clinical grounds and correlated with DNA antibody and complement levels. The disease reactivations consisted mostly of articular and cutaneous symptoms. There were 17 relapses and 22 complicating infections during the follow-up period. The levels of antibodies to native, double-stranded (ds) DNA (P less than 0.001) and antibodies to denatured, single-stranded (ss) DNA of IgG class (P less than 0.001) and C3 (P less than 0.001) correlated best with disease activity, which was estimated on the clinical symptoms and signs. These assays were not reliable, however, in predicting minor exacerbations. The levels of IgM class ss-DNA antibodies were significantly higher in SLE patients without nephritis than in SLE nephritis patients. In most cases, the combination of IgG class ss-DNA antibody and complement (C3 and CH50) determinations differentiated SLE relapse from infection.

Autoantibodies↗
PubMed1981

The absence of circulating immune complexes in patients with ankylosing spondylitis.

Sera from 50 patients with well-defined ankylosing spondylitis were examined for circulating immune complexes using both a Clq binding (fluid phase) assay and a Raji cell assay. No more than five of the patients assessed had circulating immune complexes by either one of these techniques and none were positive in both. This result is in contrast to the high prevalence in sera from unselected patients with rheumatoid arthritis and systemic lupus used as positive controls.

Adult↗
PubMed1986

Separation and characterization of complement-fixing immune complexes in juvenile rheumatoid arthritis patients.

Immune complexes (IC) in sera from patients with juvenile rheumatoid arthritis (JRA) were isolated by the use of immunoabsorbent columns. Sera from 14 JRA patients (four seropositive for 19S IgM RF and 10 seronegative, but nine having hidden 19S IgM RF) were analyzed by the anti-human Clq (alpha HClq) and anti-human C3 (alpha HC3) columns. The columns were sequentially eluted with veronal buffer, 0.02 M EDTA, 0.5 M NaCl, and 1 M propionic acid. By the alpha HClq column, IgM RF were detected in at least one of the separated IC fractions of 13 of 14 patients and IgG RF in three patients. By the alpha HC3 column, only five patients demonstrated IgM RF and only one IgG RF in the eluted fractions. On sucrose density gradient analysis (SDGA), all IC were demonstrated in the peaks greater than or equal to 19S.19S IgM RF were demonstrated by ELISA in all 14 patients, but IgG RF in only three. These studies demonstrate that complement-fixing 19S IgM RF, IgG, and IgG RF containing IC can be detected in the serum of JRA patients.

Antibodies↗
PubMed1986

Dietary bovine antigens and immune complex formation after intravenous immunoglobulin in common varied immunodeficiency.

Previously we have shown that the sera of hypogammaglobulinemic patients may contain large amounts of antigenically intact foreign protein of dietary origin, presumably due to the absence of an adequate gastrointestinal secretory immune barrier. In these studies we show that the intravenous infusion of immunoglobulin in these patients may result in high levels of immune complexes postinfusion and that at least one constituent of these complexes is likely to be bovine casein.

Agammaglobulinemia↗
PubMed1984

Deficiency in C3b receptors on neutrophils of patients with chronic granulomatous disease and hyperimmunoglobulin-E recurrent infection (Job's) syndrome.

C3b receptor (CR1) expression by neutrophils (PMNs) and erythrocytes (Es) from patients with chronic granulomatous disease (CGD) or with hyper-IgE, frequent infection (Job's) syndrome was compared with that of control subjects. The control subjects consisted of one group of patients with infections and a second group of normal, healthy individuals. Three quantitative assays were used: rosette formation with C3b-coated cellular intermediates (EAC43b), binding of radiolabeled monoclonal anti-CR1 ([125I]anti-CR1) to PMN surfaces, and binding of the antibody to nonidet P-40 (NP-40) extracts of PMNs and Es in an immunoradiometric assay. Rosette formation by the PMNs of five male CGD patients was about 50% of that of paired normal control subjects, whereas the rosette formation of three female CGD patients was similar to that of the control subjects. Surface binding of [125I]anti-CR1 to PMNs of 10 CGD patients was about half that of the normal subjects (mean percent binding was 2.33% for the CGD patients vs. 3.86% for the normal subjects, giving a difference of -1.53 +/- 0.22%, P less than 0.001 by the paired-sample t test). The degree of PMN binding was similarly low for both the male and the female CGD patients. Conversely, the binding of anti-CR1 to the PMNs of 11 infected control patients appeared to be similar to that of the normal subjects (4.51% for the patient vs. 4.21% for the paired normal subjects). The infected control group originally included four Job's syndrome patients, and when this subgroup was analyzed separately, their PMNs were shown to bind significantly less anti-CR1 than did the PMNs of the normal subjects (P less than 0.01 by the paired-sample t test). In contrast, the other infected control patients showed higher-than-normal levels of anti-CR1 binding (P less than 0.05). When compared to that of the normal subjects, the total CR1 quantitated in PMN extracts was also lower than normal in CGD patients (P less than 0.01 and in the PMN extracts of eight Job's syndrome patients tested (P less than 0.01). The PMNs of the other infected control subjects were not significantly different from those of the normal subjects in total CR1 expression. Extracts of Es from Job's syndrome patients also had fewer than normal CR1 (P less than 0.02). On the other hand, CR1 levels in E extracts from the CGD patients and the other control patients were similar to those in the normal control subjects. Quantitations of C3, C4, and factor B were normal in CGD.(ABSTRACT TRUNCATED AT 400 WORDS)

Antigen-Antibody Complex↗