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At least 505 records · Page 28Linked to original sources
PubMed1981

[Hereditary angioedema: description of a sibship and review].

Report on a newly recognized sibship with hereditary angioedema (HAE). The 27 persons investigated include 8 with decreased concentrations of C-1INH and C4 in the Serum. Three of these are children without symptoms of HAE. Five patients have characteristic attacks of HAE, some of which are predominantly abdominal. The effects of treatment with danazol in 4 patients are described. HAE is briefly reviewed with special reference to pathogenesis and treatment.

Adolescent↗
PubMed1982

Circulating antigen-antibody complexes in onchocerciasis.

The presence of circulating antigen-antibody complexes in the sera of patients with onchocerciasis was investigated using the Clq and conglutinin solid-phase binding assays. Only 50% of patients' sera had demonstrable complexes, levels of complexes were unrelated to microfilarial load and specific anti-onchocercal antibody titres and results with the two tests for complexes were not correlated. Both IgM- and IgG-containing complexes were commonly involved but there was no correlation between the levels of complexes containing these isotypes. Evidence for the presence of IgE in complexes of sera from a minority of individuals was also obtained.

Antibodies↗
PubMed1982

Complement-mediated solubilization of immune complexes in systemic lupus erythematosus.

The capacity of complement-mediated solubilization of immune complexes (complex releasing activity: CRA) was studied in 63 sera from eight systemic lupus erythematosus (SLE) patients. CRA in sera of active SLE (35 +/- 17.%) was significantly lower than that of inactive SLE (64.1 +/- 24.1%, P less than 0.001). In addition, 20 of 23 sera collected during active diseases demonstrated CRA values less than 50% of the control pooled serum. On the other hand, CRA of 29 of 40 sera from inactive disease exceeded the 50% level. CRA in SLE sera correlated with complement component levels and in particular with the CH50. Serial determination of CRA and of levels of circulating immune complexes (CIC), C4 and C3 in two active patients indicated that the correlation between CRA and the complement components was positive, while that between CRA and CIC was negative. These studies provide evidence that CRA may be useful for following the activity of SLE and that CRA reflects the levels of the complement components of both classical and alternative pathways. The possibility that CIC may be solubilized and opsonized by complement and cleared by the reticuloendothelial system was discussed.

Adrenal Cortex Hormones↗
PubMed1982

Circulating immune complexes in patients with IgA glomerulonephritis.

Fourty-four patients with IgA-glomerulonephritis (IgA GN) were studied for circulating immune complexes (IC) repeatedly in the course of disease on the evidence of four different methods suited for the detection of IC, viz. complement consumption assay, Clq-solubility test and two tests based on PEG-precipitation, and of indirect signs pointing to the presence of IC. Joint assessment of the direct and indirect signs (positivity of a minimum of 2 indirect signs or any of the direct signs) permitted to ascertain the presence of circulating IC in 72 per cent of the patients and in 63.3 per cent of the examined sera. There was no close relationship between the presence of IC and the clinical activity. On the other hand, in 16 patients positive for the rheumatoid factor (RF) the renal biopsy material revealed extensive vascular lesions. The findings suggest that the circulating IC, some of which contain RF, play a part in the pathomechanism of IgA GN and are involved in the production of the vascular abnormalities in this disease.

Adolescent↗
PubMed1982

[Immunological parameters in subjects with essential arterial hypertension. II. Serological observations].

M, G, and A immunoglobulins as well as C3 and C4 complement fractions were determined in 20 patients with essential hypertension: all the values were in the normal range. Nearly half of the patients had an abnormally high value of circulating immune complexes as determined with Clq binding assay and/or with CIC test. The rise of circulating immune complexes is not related to the stage of arterial hypertension.

Adult↗
PubMed1982

Analysis of circulating IgA and detection of immune complexes in primary IgA nephropathy.

The sera of 31 patients with primary IgA nephropathy were investigated for IgA containing immune complexes by Raji cell-binding IgA radioimmunoassay and conglutinin-binding IgA radioimmunoassay. Positive results, without correlation with IgA serum levels, were found in 68% of the patients using the first assay, in 39% of the patients with the second assay. Positive sera were analysed by gel chromatography. Conglutinin-binding IgA eluted in two peaks, a minor one of 400,000-800,000 daltons mol. wt and a major one corresponding to monomeric IgA. No increase of secretory IgA and of polymeric IgA was detectable. IgA immune complexes were likewise found in the sera of patients with systemic lupus (five of 12), rheumatoid arthritis (four of 12), subacute bacterial endocarditis (four of 12) and HB virus hepatitis (four of 16). However, the high prevalence on these sera of IgG and IgM immune complexes detected by polyethylene glycol precipitation, solid phase Clq binding assay contrasted strongly with their absence in IgA nephropathy. In addition, the presence of abnormal amounts of conglutinin reactive IgA correlated with the recurrence of IgA deposits after renal transplantation (20 patients studied). Conglutinin reactive IgA could contribute to the glomerular deposition of IgA and subsequently play a significant role in the pathogenesis of IgA nephropathy.

Antigen-Antibody Complex↗
PubMed1993

Specific induction of intracellular calcium oscillations by complement membrane attack on oligodendroglia.

Oligodendroglia (ODG) are unique among glial cell types in their capacity to activate complement in the absence of antibody, causing insertion of the potentially damaging membrane attack complex (MAC) into the plasma membrane. Using microfluorimetry of indo-1 fluorescence we have detected a complex oscillatory [Ca2+]i response in ODG following exposure to sublethal dilutions of serum-derived complement. Oscillations were transitory and preceded complete and stable return to resting [Ca2+]i levels, whereas nonoscillating ODG underwent rapid lysis. Depletion of the terminal complement component C9 from serum removed the oscillatory stimulus, which could be restored by reconstitution with purified C9. Exposure to the C9-homologous peptide melittin produced [Ca2+]i oscillations similar in pattern to those induced by whole serum. However, this type of response could not be reproduced by Ca2+ ionophores or mechanical wounding, suggesting that oscillations cannot be provoked by Ca2+ influx alone and depend on the presence of the MAC or a pore-forming lesion. Oscillations were not prevented in the continuous presence of caffeine, demonstrating independence from caffeine-releasable intracellular stores. Inhibition of the endoplasmic reticular Ca(2+)-ATPase with thapsigargin produced an abrupt elevation in [Ca2+]i but did not alter the latency between exposure to serum and the initial complement-induced transient. However, the slope of this initial transient was considerably reduced and oscillations suppressed, demonstrating dependence of the oscillatory mechanism on functional endoplasmic reticular Ca2+ stores. The coincidence of ODG recovery with oscillating [Ca2+]i suggests that the complex calcium signal that follows MAC attack may stimulate repair or protective mechanisms.

Animals↗
PubMed1996

Identification of complement activation sites in human immunodeficiency virus type-1 glycoprotein gp120.

Recombinant glycoprotein 120 (rgp120) of human immunodeficiency virus type-1 (HIV-1) activates the human complement system in the absence of anti-gp120 antibodies. HIV-1 glycoprotein gp120 can dissociate from the viral envelope either spontaneously or after binding of HIV-1 to the CD4 molecule. As a consequence, gp120 can circulate in the patient's serum and attach to the surface of uninfected CD4+ T cells. Complement activation by cell-bound HIV-1 glycoprotein gp120 with subsequent opsonization may represent a mechanism for the elimination of uninfected CD4+ cells by the reticuloendothelial system, thereby enhancing the progression of HIV disease. In the current study, the complement proteins C4,C3,C5,C9, and properdin were found to bind to a synthetic peptide covering positions 233-251 of the gp120BRU sequence on incubation with normal human serum. Complement activation by the peptide was comparable with that induced by aggregated IgG, complete rgp120, and the previously described complement-activating gp41-peptide 609-623. Activation occurred via the classical pathway and was abrogated in the presence of EDTA, Mg2+/EGTA, or C4-deficient human serum. Peptides partly overlapping the sequence 233-251 activated complement to a lesser extent. The complement-activating capacity of the gp120 sequence 233-251 was not restricted to the HIV-1BRU isolate, because a peptide from the corresponding sequence of the HIV-1MN strain was also capable of activating complement. An additional strong complement-activating site was identified in the gp120 sequence 321-360 of the HIV-1MN strain. These data indicate that distinct sites in gp120 are able to activate human serum complement via the classical pathway in the absence of anti-gp120 and independent of glycosylation.

Amino Acid Sequence↗
PubMed1996

Impaired production of both normal and mutant C1 inhibitor proteins in type I hereditary angioedema with a duplication in exon 8.

In the autosomal dominant disorder type I hereditary angioedema, reduced levels of C1 inhibitor may be due in part to increased turnover and decreased synthesis of normal C1 inhibitor protein. A type I hereditary angioedema patient was recently described in whom the C1 inhibitor mutation consisted of a 20-bp duplication of nucleotides 1414 to 1433 in exon 8 that introduced a frame shift predicting the loss of a normal stop codon and the translation of a protein 52 amino acids longer than normal. In this study, we analyzed the expression of C1 inhibitor in fibroblasts obtained from a skin biopsy of this patient. Two proteins of approximately 78 and 94 kDa were found intracellularly, corresponding to the products of normal and mutated alleles, respectively. Pulse-chase analysis showed a complete lack of secretion of the mutated form. In addition, there was decreased extracellular production of the normal C1 inhibitor, suggesting either decreased secretion or increased intracellular catabolism of the normal protein because of the presence of the mutant allele. The production of other complement proteins was normal. This study provides a model for further analysis of autosomal dominant genetic disorders in which production of the functional protein may be affected by the product of the mutated allele.

Alleles↗
PubMed1996

Routine immunologic tests in systemic lupus erythematosus: is there a need for more studies?

OBJECTIVE: To evaluate the sensitivity, specificity, and likelihood ratios of anti-dsDNA, C3, C4, and Clq binding tests for predicting flares in systemic lupus erythematosus (SLE) and to evaluate the conflicting results reported in the recent literature. METHODS: Test results from 9 to 3 months preceding 83 flares among 53 patients from a cohort study of 202 patients with SLE were assessed for their ability to predict renal and nonrenal flares and all flares combined. A flare was defined as a 6 point rise in a modified SLE Disease Activity Index. RESULTS: For all 4 tests, sensitivity approximated 50% and specificity was less than 75%. For anti-dsDNA, Clq binding, and C4, both positive and negative likelihood ratios were close to 1.0, suggesting little clinical value for routine testing. For C3, likelihood ratios for a positive test approximated 2.0, meeting the minimal level for clinical significance. Review of previous studies suggested that sample size, the use of a standardized disease activity measure to define a flare, the severity of the flare, and the study duration could not explain the discrepant results among studies. The 2 studies with testing every 4 to 6 weeks found that a rising anti-dsDNA predicted flares, while those with less frequent testing did not. CONCLUSION: While our study provided no major support for routine testing with anti-dsDNA, C3, C4, or Clq binding, additional longitudinal studies are needed to assess monthly testing of anti-dsDNA as a predictor of flare in SLE.

Adult↗