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PubMed1984

Binding capacity of sera from systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) to C3c. Evaluation by enzyme linked immunosorbent assay (ELISA).

Immunoconglutinins (IKs) are autoantibodies directed against antigenic determinants on C3 complement component. An ELISA was performed to detect IKs in sera from 50 RA patients, 50 SLE patients and 50 normal subjects. Comparison showed significantly higher levels in patients than in normal subjects (p less than 0.001) and higher IKs levels in RA than in SLE (p less than 0.001). IKs were not related to others biological tests, except a statistically significant inverse correlation between IKs and circulating immune complexes levels detected by conglutinin binding assay in RA.

Adult↗
PubMed1995

Immunofluorescence study of pemphigus from north India.

Both serum studies by indirect immunofluorescence (IIF) tests and skin biopsy examination by direct immunofluorescence (DIF) were performed on 22 cases of pemphigus with clinically active lesions. Twenty cases had pemphigus vulgaris and two, pemphigus foliaceus. The majority of cases (70%) were between 21 and 60 years old; the mean age was 39.5 +/- 12.7 years. There was no sex predilection. DIF showed the positive fluorescence of intercellular cement substance (ICS) of the epidermis in all 22 cases (100%). IgG was positive in 77.2%, followed sequentially by C3C (50%), IgA (45.45%), and IgM (36.36%). Six cases (27.27%) also showed granular immunoglobulin and/or complement deposits at the dermoepidermal junction. IIF detected serum antiepithelial antibodies in 18 cases (81.81%) using human esophagus as substrate. Most of these cases (88.88%) showed IgG type of antibodies; the other 11.11% exhibited IgA and IgM in low concentrations. 1+ titer positivity was observed in 15 cases. This study demonstrates the value of DIF for a definitive diagnosis of pemphigus. However, it is also important to appreciate that immunofluorescence is not a substitute for histopathology, but rather complementary to it.

Adult↗
PubMed1980

Sequential evaluation of immunoreactivity in patients with melanoma undergoing surgery and adjuvant therapy.

The immunologic profile of 15 patients undergoing surgery and adjuvant chemoimmunotherapy for cutaneous melanoma was studied for a mean period of 18 months. In vivo cellular immunity was assayed by evaluation of delayed hypersensitivity response (DHR) to primary antigen and a panel of recall antigens. In vitro cellular immunity was evaluated to means of total and T-lymphocyte counts in peripheral blood and by the lymphocyte blastogenic response to phytohemagglutinin stimulation. Humoral immunity was assayed by determining the serum levels of IgG, IgA and IgM and of complement components C3c, C4 and Factor B. Phagocytic activity was studied by testing leukocyte chemotaxis, neutrophil phagocytosis and leukocyte random migration. The in vitro parameters were determined preoperatively at diagnosis, 6 times during the first 2 postoperative weeks, and then every month during adjuvant therapy. No correlation was found between DHR and clinico-pathologic stage of tumor, or with subsequent clinical course. Significant depression of total lymphocyte and T-lymphocyte count and blastogenic response of lymphocytes was found at diagnosis. The lymphocyte response to PHA decreased significantly in the early postoperative period but returned to preoperative levels one week after surgery. Periodic fluctuations of lymphocyte blastogenic response and progressive decrease of total lymphocyte counts and T-lymphocyte counts were observed during the 18-month follow-up. No significant alterations of immunoglobulin levels were recorded at diagnosis or during the postoperative period. Complement levels were within normal values preoperatively; in the early postoperative period a transient increase of C3c, C4 and Factor B was recorded, then complement levels progressively decreased. Parameters of phagocytic activity were normal at diagnosis and fluctuated within the normal range throughout the whole period of study.

Adult↗
PubMed1981

Binding of fluid-phase complement components C3 and C3b to human lymphocytes.

It is known that a population of B-lymphocytes has receptors for the third component of complement, C3, and that these lymphocytes may be identified by their ability to form rosettes with sheep erythrocytes coated with covalently bound fragments of complement component C3. Human tonsil lymphocytes, enriched for B-cells, form rosettes with sheep erythrocytes coated with antibody and complement components C1, C4b and C3b (EAC143b cells). Fluid-phase C3 will inhibit rosette formation between EAC143b and human tonsil lymphocytes over the same concentration range as fluid-phase C3b. C3 is not cleaved to C3b during incubation with lymphocytes or with lymphocytes and EAC143b cells. Fluid-phase 125I-labelled C3 and 125I-labelled C3b bind to lymphocytes in a specific manner. The characteristics of binding of both radioiodinated C3 and radioiodinated C3b are very similar, but the binding oc C3 is again not a result of cleavage to C3b. Salicylhydroxamic acid does not inhibit binding of 125I-labelled C3 to tonsil lymphocytes at concentrations that completely inhibit binding of 125I-labelled C3 to EAC142 cells via the nascent binding site of C3b. It is concluded that C3 and C3b share a common feature involved in binding to lymphocytes bearing receptors for the third component of complement.

Animals↗
PubMed1977

Pathogenetic factors in utricaria in children. A clinico-experimental study.

Results of a study in 62 patients with urticaria and 30 controls, all under 12 years of age, are reported. The study involved history taking and assays of immunoglobulins A, G, M, D, E, of complement fractions C3c and C4 and estimation of C1 estease inactivator activity in the plasma. Acute urticaria is more frequent than chronic urticaria in children, expecially in subjects with atopic diathesis; papular urticaria (or strophulus infantum) is particularly frequent in children under 6 years of age and in the male. Assays of plasma immunoglobulins demonstrated selective deficiency of IgA in two and significant reduction of this immunoglobulin in a further three cases. The mean levels of IgE proved normal in chronic urticaria, raised in acute urticaria, and very high in papular urticaria. Complement assays demonstrated, in one case, a reduction of C3c below 60 mg/100 ml, persisting after the disappearance of urticaria.

Acute Disease↗
PubMedDate not supplied

C3c-binding in inflammatory rheumatic diseases.

Sera from 73 patients, 24 with rheumatoid arthritis (RA), 10 with Sjögren's syndrome (SS, 4 with and six without RA), 17 with Reiter's syndrome (RS), 10 with systemic lupus erythematosus (SLE), 9 with Yersinia arthritis (YA), and 3 with mixed connective tissue disease (MCTD) were examined by enzyme-immunoassay (EIA) for the presence of C3c-binding IgG, IgM, and IgA activity (C3cBIgG, C3cBIgM, C3cBIgA). This activity probably consists of immunoconglutinins and immunoglobulin aggregates. Significantly elevated C3cBIgG was found in the sera of patients with RA (p less than 0.01), SS, and SLE (p less than 0.02). C3cBIgM was elevated in SS and SLE (p less than 0.02). C3cBIgA was increased in RA (p less than 0.005), in SS and YA (p less than 0.02). Correlations of C3c-binding with erythrocyte sedimentation rate, hemoglobin, C-reactive protein, IgG-binding onto platelets, serum IgG, IgM, and IgA levels, and with rheumatoid factors of IgM and IgA classes were computed. C3cBIgG, C3cBIgM, and C3cBIgA correlated significantly with each other, but usually not with other laboratory variables. The exceptions were positive correlations of C3cBIgM with IgM-rheumatoid factors in RA (p less than 0.05), and with serum IgM levels in the whole series of patients (p less than 0.05). The use of C3c represents a new principle to detect abnormalities in the sera of patients with inflammatory rheumatic diseases. However, the pathogenic significance of elevated C3c-binding remains unknown.

Complement C3↗
PubMed1996

Complement in acute and chronic arthritides: assessment of C3c, C9, and protectin (CD59) in synovial membrane.

OBJECTIVES: To investigate the role of complement cascade induced damage and protection against it in acute arthritides compared to rheumatoid arthritis and other chronic joint derangements. METHODS: C3c, C9, and protectin (CD59) were examined by avidin-biotin-peroxidase complex staining. RESULTS: Marked deposits of C3c and C9 were found in synovial vasculature and intercellular matrix of the lining in rheumatoid arthritis and in acute arthritides (including bacterial, reactive, and osteoarthritis flare up). Furthermore, protectin was not visible in synovial lining cells and was relatively weakly expressed in stromal and endothelial cells in rheumatoid arthritis; also in acute arthritides protectin expression was weak. In contrast, C3c and C9 deposits were not found in chronic conditions associated with degenerative diseases (osteoarthritis and osteochondritis dissecans) or mechanical causes (patellar luxation and a ruptured meniscus), in which also the protectin expression was prominent in synovial lining, endothelial and some stromal cells. CONCLUSIONS: Activation of the complement in rheumatoid arthritis and in acute arthritides seems to be associated with a decreased protection of synovial cells against cellular effects and lysis mediated by membrane attack complex.

Acute Disease↗
PubMed1989

Characterization of receptors to the anaphylatoxins on isolated cells.

The anaphylatoxins exhibit three primary functions in vivo, i.e. they induce granulocyte sequestration and adherence, promote spasmogenesis or smooth muscle contraction and exert immunoregulatory influences. C5a receptors have been demonstrated on human neutrophils, human monocytes, rodent macrophages from both the lungs and peritoneal cavity, two mouse macrophage cell lines (RAW 264 and J774.A1) and guinea pig platelets. To date, only guinea pig platelet has been shown to possess C3a receptors. In depth studies with the rat mast cell have demonstrated that both direct and indirect activation mechanisms may be operative in the mast cell; however, neither mechanism appears to depend on receptor-mediated stimulation of these cells.

Anaphylatoxins↗
PubMed1991

[Behavior of granulocytic receptors for Fc IgG fragment and C3 component of complement in patients with diabetes].

The count of peripheral neutrophils having the superficial receptors for Fc IgG fragment (FcR) and C3 component of the complement (CR) was determined in diabetic patients by using the rosette tests EA and EAC according to the modified Buescher method. A significantly lower percentage of neutrophils with FcR and CR receptors was found in patients with both insulin-dependent and noninsulin-dependent diabetes. The lowest values were found in noncompensated diabetes; in compensated diabetes they were higher but still significantly lower than in the controls. The difference was significant in both tests used. The results obtained suggest that the observed fall in the percentage of neutrophils with FcR and CR receptors is caused by metabolic disturbances associated with diabetes.

Complement C3c↗
PubMed2001

Evaluation of a system for the perfusion of isolated, rodent organs.

Perfusion of isolated organs is a common experimental approach. However, the surfaces of the perfusion system might alter the components of the blood and thereby negatively affect organ function. The aim of this study was to minimize the influence of the perfusion system on the blood components and to evaluate the system. Pressure and flow in the perfusion system consisting of a roller-pump, reservoir, oxygenator, hemo-filter and bubble-trap with a total tubing length of 4.5 m are controlled by a computer software (DASYLAB, Datalog, Moenchengladbach, Germany) via a transducer connected to the system. The organ to be perfused is positioned under a microscope (Orthoplan, Leica, Bensheim, Germany), allowing the investigation of microcirculatory parameters. The images raised are recorded on video tapes. To evaluate the system it was perfused with human blood (Hct 28 to 30%) for 90 min. Heparin (n = 6) or citrate (n = 6) served as anti-coagulants. The disappearance of cells from the blood was determined at time points 0, 1, 5, 10, 15, 20, 30, 45, 60, 75 and 90 min by means of a cell counter (AC T8, Coulter Beckmann, Krefeld, Germany). Cell activation was assessed by analysis of the expression of L- and P-selectin and CD11b. The activation of the complement system was examined by measuring the serum levels of the complement factors C3c and C4. There was no significant loss or activation of the blood cells at any of the above given time points. The serum levels of the complement factors remained within the physiological range and showed no changes throughout the whole experiments. Thus, the perfusion system does not have a negative influence on the blood and its individual components, and is therefore a reliable tool for perfusion experiments.

Acute Disease↗
PubMed2000

Effects of new polymer-coated extracorporeal circuits on biocompatibility during cardiopulmonary bypass.

An inflammatory response due to bioincompatibility of extracorporeal circuits is a major clinical issue during cardiopulmonary bypass (CPB). By using a swine model, we determined whether new polymer-coated circuits, the blood-contacting surfaces of which are coated with poly(2-methoxyethylacrylate) (PMEA), would reduce the inflammatory response during CPB. Plasma bradykinin levels and the percentages of CD35-positive monocytes in PMEA-coated circuits were significantly lower than those in uncoated circuits during CPB. The amount of proteins adsorbed on the PMEA-coated circuits was significantly lower than that on the uncoated circuits (0.30 microg/cm2 versus 3.42 microg/ cm2). Almost no IgG, IgM, or C3c/d was detected in proteins adsorbed on the PMEA-coated circuits although these proteins were clearly detected in proteins adsorbed on the uncoated circuits. We concluded that PMEA coating could reduce complement activation during CPB by suppressing the adsorption of IgG and IgM, which activate C3 via the classical pathway, on the surface of the circuits.

Acrylates↗
PubMed1996

Leucocytoclastic vasculitis induced by prolonged exercise.

Many people develop skin symptoms after long-distance walks, but little is known about the aetiology of these. In this study we took 11 biopsies from 10 long-distance walkers who walked 80 km. All biopsies originated from purpuric lesions on the lower legs, which had appeared during walking. In all 11 specimens, signs of a leucocytoclastic vasculitis were present with leucocytoclasis, exocytosis of erythrocytes and a granulocyte/mononuclear perivascular infiltrate. Immunofluorescence investigations showed deposition of C3c in many specimens and immunoglobulin M in some. The occurrence of a leucocytoclastic vasculitis after prolonged exercise may be explained by the existence of an exercise altered cutaneous microcirculation, complement activation and an altered immune function.

Complement C3c↗
PubMedDate not supplied

C-type lectins and galectins mediate innate and adaptive immune functions: their roles in the complement activation pathway.

In recent years, a 'new' pathway for complement activation mediated by the mannose-binding lectin (MBL) has been described as a key mechanism for the mammalian acute phase response to infection. This complement activation pathway is initiated by a non-self recognition step: the binding of a humoral C-type lectin [mannose-binding lectin (MBL)] to microbial surfaces bearing 'foreign' carbohydrate determinants. The recognition factor, MBL, is associated with a serine protease [MBL-associated serine protease (MASP)] which, upon MBL binding to the microbial ligand, activates the complement component C3, leading to either (a) phagocytosis of the opsonized target via the complement receptor, or (b) humoral cell killing via assembly of the membrane attack complex. Galectins (formerly known as S-type lectins) modulate activity of the complement receptor 3 (CR3), the macrophage membrane receptor for complement components C3b and iC3b, downstream products of the MBL pathway which are covalently bound to 'target cells. Galectins also mediate macrophage- and dendrocyte-adhesion to lymphocytes activated by signaling through another C-type lectin, the L-selectin, leading to immunoglobulin-mediated responses. Thus, the functional interplay of MBL, galectins and L-selectin in the acute phase response neutralizes the microbial challenge, and lead to further adaptive immunity. Although the observation of various components of the lectin pathway in different invertebrate species demonstrates the high conservation and ancient roots of the components of innate immunity, there has previously been no evidence supporting the possibility that the integral lectin-mediated complement activation pathway is present in invertebrates. We now have evidence for the coexistence of homologs of all the pathway's key components (MBL, MASP, C3, and galectin) in the protochordate Clavelina picta, suggesting the lectin-mediated pathway of complement activation preceded the immunoglobulin pathway in evolution. Therefore, despite being 'new' to the textbooks, experimental evidence indicates that this pathway is ancient, and has been conserved intact throughout its evolution.

Amino Acid Sequence↗
PubMed1991

Plasma C3c in immune-mediated neurological diseases: a preliminary report.

Plasma C3c levels were examined in 56 patients with immune (27) and non-immune (29) mediated neurological diseases by crossed immunoelectrophoresis. Plasma samples were collected during the active phase of illness in both groups, usually within 7 days of admission. 11 patients (4 Guillain-Barré Syndrome-GBS, 3 chronic inflammatory demyelinating polyneuropathy-CIDP, 4 myasthenia gravis-MG) had their plasma saved sequentially during the active and the recovery phase. Plasma C3c levels were elevated in the group with immune mediated diseases when compared with those of non-immune mediated diseases. The sensitivity and specificity of C3c as a diagnostic test for immune mediated neurological diseases were 61.4 and 100% respectively with a positive and negative predictive value of 100 and 41%. the C3c levels in plasma correlated well with disease severity in MG and GBS patients. Such a correlation was also evident in all CIDP patients except one that had persistent elevation in the presence of clinical improvement. Results suggest that the plasma C3c level may be useful for differentiating immune from non-immune mediated neurological diseases. Plasma C3c may also be used for monitoring disease severity, particularly in myasthenia gravis.

Autoimmune Diseases↗
PubMed1993

Complement activation during extracorporeal circulation. In vitro comparison of Duraflo II heparin-coated and uncoated oxygenator circuits.

The degree of complement activation during cardiopulmonary bypass is considered a valuable parameter of biocompatibility of the extracorporeal circuit. In an in vitro setting with a heart-lung machine primed with fresh whole blood and saline solution, the C3 activation products C3b, iC3b, and C3c and the terminal complement complex were measured in double-antibody enzyme immunosorbent assays. No differences were found between seven sets treated with Duraflo II heparin coating and seven uncoated sets after 2 hours of circulation. C3 activation products (expressed as median and 95% confidence intervals) increased from 4.5 AU (2.8 to 12.3 AU) to 16.5 AU (10.0 to 19.4 AU) in the uncoated sets (p = 0.02) and from 4.6 AU (2.2 to 5.8 AU) to 19.3 AU (3.5 to 27.1 AU) in the coated sets (p = 0.02). Terminal complement complex increased from 5.7 AU (2.7 to 11.3 AU) to 13.6 AU (8.2 to 17.8 AU) in the uncoated sets (p = 0.02) and from 7.9 AU (4.6 to 11.4 AU) to 17.3 AU (9.4 to 35.1 AU) in the coated sets (p = 0.02). A significant drop in thrombocyte levels was observed in both coated and uncoated sets. In a supplementary series, the sterilization process did not influence the results. Although Duraflo II heparin coating is considered highly effective in preventing coagulation, it did not prevent complement activation in the present in vitro study. We hypothesize that the mode by which the heparin molecule is bound to the surface may be essential to obtain effects on both coagulation and complement system.

Biocompatible Materials↗