An extended C1q-binding assay using lactoperoxidase- and chloramine-T-iodinated C1q. Immediate distinction between immune-aggregate-mediated and non-immune-aggregate-mediated C1q binding.

An extension of the C1q-binding assay for the detection of immune-aggregate-mediated and non-immune-aggregate-mediated C1q binding is reported. The assay involves the use of two different C1q preparations, one radioiodinated by means of lactoperoxidase (LPO-125I-C1q) and the other by means of chloramine-T (CT-125I-C1q). The treatment with CT for 20 min at room temperature before iodination for 1 min led to abolishment of the C1q-binding capacities to complexed IgG: approximately 50% of LPO-125I-C1q but only 2% of CT-125I-C1q bound to 80 micrograms/ml of IgG forming part of tetanus toxoid/anti-tetanus toxoid complexes or to 200 micrograms/ml of heat-aggregated human gamma globulin. Similar results were obtained with staphylococcal protein-A-aggregated IgG. CT-treated C1q was haemolytically inactive. In contrast to the results with complexed IgG, CT treatment did not markedly reduce binding capacities of C1q to heparin: approximately 55% of LPO- and CT-125I-C1q were bound by 127 U/ml of commercial heparin in normal human serum. Both C1q preparations bound to a comparable extent to fibronectin, fibrinogen, and various bacterial endotoxins. When the LPO- and CT-125I-C1q-binding patterns obtained on serum samples from patients with systemic lupus erythematosus, rheumatoid arthritis, or essential mixed cryoglobulinaemia were compared with binding patterns observed using laboratory reactants, an immediate detection of non-immune-aggregate-mediated C1q binding became possible.

Symmetrical reactive oligoarthritis after Campylobacter jejuni enteritis--case report and study of the synovial complement.

A 34-year-old man, in whom sacroiliitis had been diagnosed 5 years previously, presented in July 1982 with reactive arthritis following Campylobacter jejuni enteritis. Diarrhoea was stopped by erythromycin but joint effusion recurred. In order to clarify the relationship between Campylobacter jejuni and the immunological system, we proceeded with a study of the synovial complement. The results were compared with those obtained in some other arthropathies.

Complement activation and impaired capacity to solubilize immune complexes or to prevent their formation in essential mixed cryoglobulinemia.

The complement profile, the immune complex solubilizing capacity (ICSC), the immune complex precipitation inhibition capacity (ICPIC), the presence of cryoprecipitable material, and the presence of immune-aggregate- and non-immune-aggregate mediated C1q-binding activity was assessed in serum samples from 23 patients suffering from essential mixed cryoglobulinemia (EMC). No correlation between the levels of cryoglobulins and the clinical activity of EMC was found. The mean C1q-binding activity in EMC serum samples was abnormally elevated 28 +/- 29% (mean +/- SD). In six out of eight serum samples that contained C1q-binding material, evidence was obtained that such material was of the complexed immunoglobulin G (IgG) type. Among the levels of C1q, C1r, C2, C4, C3, C5, C6, C1-inhibitor, C3d, B, I, H, as well as the total hemolytic activity and the activity of the alternative pathway of the complement, the mean serum concentrations of C1, C2, and C4 and in consequence the mean total hemolytic activity were significantly reduced, whereas the mean levels of C3d were significantly elevated in the EMC serum samples. The capacity of the 23 EMC serum samples to solubilize preformed immune precipitates from bovine serum albumin (BSA) and rabbit anti-BSA antibodies as well as their capacity to prevent the formation of the precipitable form of such complexes was analyzed. Compared to the ICSC and the ICPIC of 30 normal human sera, the ICSC and the ICPIC of EMC serum samples were reduced to 57 +/- 24% and 38 +/- 33%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)