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PubMed1983

C3 cleavage products stimulate release of prostaglandins by human mononuclear phagocytes in vitro.

Human monocytes cultured for up to 48 hr in serum-free, chemically defined culture media released low levels of prostaglandin. C3b, C3bi, and C3c stimulated an indomethacin-sensitive, dose-responsive increase in the amount of monocyte prostaglandin released by 18 hr after treatment. Native C3 and C3d, which do not bind to monocyte receptors, failed to stimulate increased prostaglandin release. Lymphocytes, treated and untreated, produced 10(-2) to 10(-3) as much prostaglandin as the monocytes. These data support the concept that monocytes are a significant source of leukocyte prostaglandin. They also introduce an important new biologic function for the C3 fragments C3b, C3bi, and C3c.

Cells, Cultured↗
PubMed1991

Immunopathology of subcutaneous rheumatoid nodules.

Nodules obtained from five patients with classical seropositive rheumatoid arthritis were studied by an immunofluorescence technique using polyclonal antibodies to IgG, IgA, IgM, C3c, and fibrin, and monoclonal antibodies to the terminal (C5b-9) complement complex (reaction with a neoantigen in C9 revealed during activation), DR antigens, T cells, macrophages, and interdigitating cells. In all instances the central necrotic areas stained strongly for fibrin and more weakly for IgG, IgA, IgM, C3, and terminal complement complex. The surrounding palisading cells reacted with antibodies to DR and macrophages. In the peripheral granulomatous tissue most of the lymphocytes reacted with the antibodies to T cells, whereas various amounts of the larger mononuclear cells were stained by antibodies to DR antigens, macrophages, and interdigitating cells. In all instances the walls of some of the smaller vessels in the granulomatous tissue stained for fibrin, C3, and terminal complement complex. Plasma cells were not seen except for scattered IgM cells in one nodule. These results support the view that the palisading cells are derived from macrophages, and indicate that there is vasculitis with activation of C3 and the terminal complement pathway in the granulomatous tissue.

Arthritis, Rheumatoid↗
PubMed1986

In situ characterization of the inflammatory cell infiltrates of hyperplastic denture stomatitis.

Cryostat sections from 14 surgical specimens were examined to determine whether selected factors of the immune response related to histopathological reactions are present in the palatal mucosa affected by hyperplastic denture stomatitis. By means of various immunological techniques the presence of IgG, IgA, IgM, complement factor C3c, receptors for the Fc region of IgG (FcR) and for complement factor C3b (C3bR), T lymphocytes, and macrophages were studied. The inflammatory infiltrate was mainly located in the papillary part of the lamina propria. IgG, IgA, and IgM appeared both in plasma cells and intercellularly. FcR, C3bR, and T lymphocytes were present in the areas with inflammatory cell infiltrate. Macrophages were found in the papillary part of the lamina propria and within the epithelium. The immunological response in the mucosa affected by denture stomatitis was in many respects similar to that of marginal and apical periodontitis. We conclude that hyperplastic denture stomatitis is a complex inflammatory lesion showing elements of both humoral and cellular immune responses.

Antibody Formation↗
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↗
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↗
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↗
PubMed1991

Pre-ligation of CR1 enhances IgG-dependent phagocytosis by cultured human monocytes.

Opsonization of the C3b receptor (CR1) on phagocytic cells with C3b enhances both attachment of targets to the cells and subsequent IgG-dependent ingestion of these targets. To explore mechanisms involved in this increased phagocytosis, we adhered cultured human monocytes to surfaces pre-coated with CR1 ligand or control proteins and quantitated ingestion of sheep E opsonized with IgG alone. Three ligands for CR1 resulted in markedly enhanced phagocytosis of targets when compared individually to a panel of non-ligands, as determined by both the proportion of monocytes ingesting targets (percent phagocytosis) and by the number of targets ingested per 100 monocytes (phagocytic index). The ligands included purified C3b, iC3, and Fab fragments of 1B4, a monoclonal anti-CR1, which resulted in a percent phagocytosis of 56.3 (p less than 0.01), 59.0 (p less than 0.01), and 54.4 (p less than 0.02) and a phagocytic index of 281.2 (p less than 0.01), 281.1 (p less than 0.01), and 247.1 (p less than 0.02), respectively. Control proteins including human serum albumin, hemoglobin, Fab fragments of anti-fibronectin, anti-beta 2 microglobulin, and MOPC 21, and Fc fragments of 1B4 and MOPC 21 produced no significant stimulation of phagocytosis, nor did F(ab')2 fragments of monoclonal anti-CR3, M1/70. CR1-specific augmentation of target ingestion was apparent with monocytes cultured in serum-free medium for 1 to 7 days, but was not seen with freshly elutriated cells. Phagocytosis of unopsonized or IgM-coated targets was minimal. These results suggest that the adherent monocytes are primed by CR1 cross-linking for enhanced FcR-mediated phagocytosis even when the CR1 ligand is not present on the targets. This contrasts with the behavior of CR3, and demonstrated functional divergence between these C3 fragment receptors in the phagocytic process.

Antibodies, Monoclonal↗
PubMed1988

Age- and sex-specific pediatric reference intervals: study design and methods illustrated by measurement of serum proteins with the Behring LN Nephelometer.

We analyzed blood from 450 healthy children and adolescents, ages one to 19 y, as well as term and preterm infants, to define age- and sex-specific reference intervals for numerous blood constituents. Reference intervals were derived by using nonparametric methods to determine the 0.025 and 0.975 fractiles. Ten serum proteins were measured with the Behring LN Nephelometer. Girls over 10 years of age had higher concentrations of ceruloplasmin and alpha 1-antitrypsin than other children had. There was no sex-related difference in reference intervals for the other proteins tested. Reference intervals are presented for immunoglobulins G, A, and M, complement fractions C3c and C4, ceruloplasmin, transferrin, alpha 1-antitrypsin, retinol-binding protein, and prealbumin (transthyretin).

Adolescent↗