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PubMed1976

Further characterization of protein A reactive and non-reactive subfragments of Fc from human IgG.

Tryptic digests of acid-treated Fc from normal human IgG were separated into four peaks (I-IV) by gel filtration on Sephadex G-100. The second peak was further divided into two fractions (II and II'). Peak I was indistinguishable from intact Fc on electrophoresis, immunodiffusion, and reactivity to protein A. The protein A reactive fragments of fractions II, II', and III were shown to contain antigenic determinants of both the CH2 and CH3 domains, to interact with the anti-Gm (1) specific rheumatoid factor, and to fix complement. These results, together with SDS-electrophoresis, showed that protein A reactive fragments are all composed of an intact Fc chain with shorter chains covalently linked to it. The protein A non-reactive fragments of fractions II' and III were homogeneous, fixed complement and showed no interaction with the Gm (1) rheumatoid factor. These results, in addition to the observed antigenic determinants, localized the fragments to the CH2 region.

Bacterial Proteins↗
PubMed1977

Binding of aggregated IgG to nephritogenic type 12 streptococci: influence of serum, C1 and C4.

The uptake of aggregated IgG by type 12, M protein positive (M + ve) streptococci was high in the presence of fresh serum, while the uptake by type 12, M-ve, type 1 and type 2, M + ve or M-ve streptococci was inhibited. Serum heated to 56 degrees C for 30 min inhibited the uptake of aggregated IgG by all strains tested. Purified C1q or macromolecular C1 added to heat-treated serum restituted the uptake of aggregated IgG. It was shown that C1 and C4 in fresh serum influenced the uptake of aggregated IgG by streptococci, resulting in the distinct reaction patterns observed.

Binding Sites, Antibody↗
PubMed1981

Complement-dependent in vitro cytotoxicity against autologous invasive bladder tumor cells in humans. Evaluation of the possible role of naturally-occurring antibodies in complement-dependent cytotoxicity.

Complement-dependent serum-mediated cytotoxicity (CDC) was measured in a 51-chromium release assay against autologous tumor cells from 7 non-invasive and 9 invasive transitional-cell tumors of the urinary bladder. CDC was demonstrated against tumor cells from invasive tumors. Heat-inactivation of autologous sera lead to complete loss of cytotoxicity. There were no differences in CDC of autologous sera from patients and allogenic sera from controls. The cytotoxic response seems to be strongly dependent on the target cell. CDC was significantly reduced by use of an allogenic C 2 deficient serum. Direct immunofluorescence did not reveal any tumor cell associated immunoglobulins of IgG or IgM classes. Indirect immunofluorescence with autologous heat-inactivated sera demonstrated in most cases both IgG and IgM attachment to the tumor cells, but there were no obvious relations between indirect immunofluorescence and CDC. Absorption of allogenic sera to trypsin- or neuraminidase-treated erythrocytes did not affect CDC of these sera against invasive tumor targets. The results indicate a complement-dependent cytotoxicity against target cells from invasive bladder tumors. Complement seems to be activated through the classical pathway, but the possible role of naturally-occurring antibodies against invasive tumor targets is not clarified.

Aged↗
PubMedDate not supplied

C4 and HLA haplotypes associated with partial inhibition of anti-Rg and anti-Ch.

Rg and Ch typing was performed, by serum inhibition, on 145 families that had been typed for HLA/C4/BF/C2 with a view to assessing partial inhibition (p.i.) of anti-Rg/Ch and its haplotype associations. Rg p.i. was found predominantly with the C4A*3A*2,B*QO homoduplicated C4 haplotype and BFF. The original type of Ch p.i. (Nordhagen et al., 1980) was closely associated with the allotype C4B 2, which also occasionally exhibited complete inhibition (c.i.), but this Ch p.i. was also found with the C4A*1,B*QO haplotype (Rittner et al., 1984a). The second type of Ch p.i. (Giles, 1984) was closely associated with the C4B 1 allotype most frequently in the haplotype C4A*6,B*1 but also with C4A*3,B*1. Both types of Ch p.i. are usually found with BF S. The present data indicate that the determinants of Rg and Ch are not directly related to any particular C4 allotype or extended haplotype. Further examples of C4A 1 with Ch and C4B 5 without Ch determinants have been detected and theoretical considerations are discussed as to how they might have arisen from unequal crossovers in homologous regions that result in hybrid protein molecules.

Alleles↗
PubMed1997

A macrophage invasion mechanism of pathogenic mycobacteria.

Tuberculosis is the leading cause of death due to an infectious organism, killing an estimated 3 million people annually. Mycobacterium tuberculosis, the causative agent of tuberculosis, and other pathogenic mycobacteria require entry into host macrophages to initiate infection. An invasion mechanism was defined that was shared among pathogenic mycobacteria including M. tuberculosis, M. leprae, and M. avium but not by nonpathogenic mycobacteria or nonmycobacterial intramacrophage pathogens. This pathway required the association of the complement cleavage product C2a with mycobacteria resulting in the formation of a C3 convertase. The mycobacteria-associated C2a cleaved C3, resulting in C3b opsonization of the mycobacteria and recognition by macrophages.

Amino Acid Sequence↗
PubMed1986

Regulation of class III major histocompatibility complex gene products by interleukin-1.

Interleukin-1 (IL-1) is a product of mononuclear phagocytes that mediates changes characteristic of the response to inflammation or tissue injury (the acute-phase response). One of two structurally and functionally homologous major histocompatibility complex (MHC) class III genes encodes a positive acute-phase protein, complement factor B. The closely linked complement C2 gene is not affected during the acute-phase response. Purified human IL-1, pH 7.0, and recombinant-generated murine IL-1, pH 5.0, increased the expression of factor B and other positive acute-phase proteins in human hepatoma cells but decreased the expression of albumin, a negative acute-phase reactant. Furthermore, in a murine fibroblast L-cell line transfected with cosmid DNA bearing the human C2 and factor B genes, IL-1 mediated a reversible dose- and time-dependent increase in factor B expression in the transfected cells. Expression of the C2 gene was not affected by IL-1. The effect of IL-1 on factor B expression involves a mechanism acting at a pre-translational level as demonstrated by an increase in specific messenger RNA content and a corresponding increase in biosynthesis and secretion of factor B. The structural basis and mechanism for selective and independent regulation of these genes provides insight into the molecular control of the inflammatory response.

Animals↗
PubMed1977

Influence of serum-derived chemotactic factors and bacterial products on human neutrophil chemotaxis.

The chemotaxis of neutrophils has been shown to be modulated by serum factors, tissue factors, bacterial products, and a host of other substances. In vivo, these factors may act in concert with each other to modify neutrophil movement. We examined the effect of aggregated gamma globulin-activated serum (AS), bacterial factors, and endotoxin either alone or in combination with each other, on human neutrophil chemotaxis. Exposure of neutrophils to AS resulted in deactivation to AS but not to Escherichial coli or Staphylococcus epidermis culture filtrate. Exposure of neutrophils to S. epidermis or E. coli CF or E. coli endotoxin resulted in deactivation to AS or C5a but not to E. coli or S. epidermis culture filtrate. Addition of endotoxin to AS or C5a resulted in inhibition of chemotaxis by untreated neutrophils toward this combination as compared with AS alone. These results suggest that separate mechanisms may be involved when serum or bacterial chemotactic factors initiate human neutrophil chemotaxis. Furthermore, the potent but specific inhibitory effect of endotoxin on chemotaxis toward AS may be of clinical significance.

Blood↗
PubMed1992

Legionella pneumophila lipopolysaccharide activates the classical complement pathway.

Legionella pneumophila is a gram-negative bacterium capable of entering and growing in alveolar macrophages and monocytes. Complement and complement receptors are important in the uptake of L. pneumophila by human mononuclear phagocytes. The surface molecules of L. pneumophila that activate the complement system are unknown. To identify these factors, we investigated the effects of L. pneumophila lipopolysaccharide (LPS) on the classical and alternative complement pathways of normal human serum by functional hemolytic assays. Although incubation of LPS in normal human serum at 37 degrees C resulted in the activation of both pathways, complement activation proceeded primarily through the classical pathway. Activation of the classical pathway by LPS was dependent on natural antibodies of the immunoglobulin M class that were present in various quantities in sera from different normal individuals but were absent in an immunoglobulin-deficient serum obtained from an agammaglobulinemic patient. Additional studies using sheep erythrocytes coated with LPS suggested that the antibodies recognized antigenic sites in the carbohydrate portion of LPS. The ability of LPS to interact with the complement system suggests a role for LPS in the uptake of L. pneumophila by mononuclear phagocytes.

Complement C1↗
PubMed1994

Type C retrovirus inactivation by human complement is determined by both the viral genome and the producer cell.

The inactivation of type C retroviruses by human serum may be a considerable impediment to the use of retroviral vectors in vivo for gene therapy. Here we show that virus inactivation is dependent both on the virus and on the cell line used to produce the virus. All viruses produced from murine NIH 3T3 or dog Cf2ThS+L- cells are sensitive to human serum. In contrast, those produced from mink Mv-1-Lu and human HOS or TE671 cells are at least partially resistant, with the exception of murine leukemia viruses. In particular, the feline endogenous virus RD114 is completely resistant to a panel of eight human sera when produced from Mv-1-Lu or HOS cells. This differential resistance is controlled by the viral envelope proteins. Virus inactivation can be correlated with the ability of the producer cells to be lysed by human serum. Inactivation of sensitive viruses requires the classical pathway of complement but does not require virion lysis.

3T3 Cells↗
PubMed1994

HLA-B alleles and complotypes in Mexican patients with seronegative spondyloarthropathies.

OBJECTIVES: To analyse major histocompatibility complex (MHC) haplotypes in Mexican mestizo patients with seronegative spondyloarthropathies (SSpA) and normal controls, to discover if there are other antigens, besides B27, in the HLA region that might show association with the disease. METHODS: The study included 100 Mexican mestizo patients with SSpA and 200 of their first degree relatives. These groups were compared with 85 ethnically matched controls. The class I and class III MHC antigens were obtained by standard methods. The significance of differences between patients and controls was tested by chi 2 analysis; linkage disequilibrium among the different alleles in each haplotype was estimated by computing delta values. RESULTS: We found a significantly increased frequency of the HLA-B27 antigen (pcorr. = 1 x 10(-5), odds ratio (OR) = 33.4, 95% confidence interval (CI) = 9.3-142.0). In the group of 45 SSpA patients negative for the B27 antigen, independent increased frequencies of HLA-B49 antigen (pcorr. = 0.03, OR = 6.5, 95% CI = 1.5-32.8)) and the FC31 complotype (pcorr. = 0.04, OR = 3.7, 95% CI = 1.2-11.1) were found. Significant delta values were obtained for the [B27;SC30] haplotype (p = 0.0005) but not for haplotypes marked by the FC31 complotype. HLA-B antigens on the homologous chromosome in B27 positive patients were mainly HLA-B51 (18%) and HLA-B60 (16%); however, the observed genotypes B27/B51 and B27/B60 were not significantly different than expected from the allele frequencies alone. CONCLUSIONS: These data suggest that in Mexicans additional genes within the MHC region besides the HLA-B27 antigen, might be related to the genetic susceptibility for developing SSpA. Relevant antigens included the HLA-B49 and the FC31 complotype.

Adult↗
PubMed1975

Complement.

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Anaphylaxis↗
PubMed1983

Infections and hypocomplementemia.

The complement system, phagocytic leukocytes, and antibodies constitute the "department of defense" in the battle against infections caused by pyogenic microorganisms. Complement components are capable of directly killing (by lysis) certain susceptible bacteria and are the source of chemotactic peptides and heat-labile opsonin, which facilitate recognition and killing of microbes by phagocytic cells. When these vital functions are compromised, as in individuals with inherited deficiencies of complement components, the result is unusual susceptibility to severe infections.

Complement Activation↗
PubMed1986

Inherited complement component abnormalities.

Inherited deficiencies of early complement components are frequently associated with immune/rheumatic disorders and recurrent (Neisserial) infection with deficiency of late complement components. The genetic complexity of complement components is further demonstrated by electrophoretic allotypy and analysis of DNA restriction fragment length polymorphisms.

Adult↗