A method to differentiate between anti-C1q antibodies and C1q-binding immune complexes using collagenase-digested solid phase C1q.

A method for the detection of circulating immune complexes in the presence of autoantibodies to C1q is described. Solid phase C1q-digestion with bacterial collagenase results in the elimination of the collagen-like region of C1q. Binding of model immune complexes to this modified solid phase C1q is practically unaltered, while reactivity of anti-C1q antibodies is abolished by this procedure. In conjunction with an ELISA using the collagen-like region of C1q as antigen this modified C1q solid phase assay may be used to determine immune complexes and anti-C1q antibodies in the sera of patients with autoimmune rheumatic diseases.

Racial differences in antinuclear antibody patterns and clinical manifestations of scleroderma.

The profile of antinuclear antibodies (ANA) in 49 Thais with scleroderma (systemic sclerosis) was compared with that in 68 white Australians with scleroderma. Forty-eight (98%) of the Thais and all (100%) of the white Australians were positive for ANA, with the majority (100% and 97%, respectively) showing a diffuse speckled pattern of nuclear fluorescence. The distribution of the patterns was different in the 2 races; 35 (71%) of the Thais and 17 (25%) of the Australians showed staining of the nucleolus, and 1 (2%) of the Thais and 35 (51%) of the Australians showed staining of the centromeres. The frequency of precipitating antibodies to extractable nuclear antigens was also strikingly different: 86% in Thais and 26% in Australians (P less than 0.001). Precipitating antibodies to Scl-70 (topoisomerase I), the predominant extractable nuclear antigen in patients with scleroderma, were detected in 37 (76%) of the Thais and 18 (26%) of the Australians, and these were shown by Western blotting to react with the Scl-70 (topoisomerase I)-associated polypeptides. Differences in the frequencies of the ANA specificities in the 2 races were consistent with differences in the clinical manifestations of scleroderma; all of the Thai patients, in contrast to 15% of the Australian patients, had diffuse scleroderma with widespread skin involvement. This suggest that environmental or genetic factors may influence the expression of scleroderma.

Disseminated infection with Conidiobolus incongruus.

The first fatal case of disseminated infection due to Conidiobolus incongruus is reported. The patient presented with a subcutaneous mass, febrility, weight loss, cough and hemoptysis. Histological examination of skin and subcutaneous tissue, lung, lymph nodes, esophagus, liver and jejunum showed a granulomatous reaction with bright eosinophilic amorphous material and broad hyphae. A fungus cultured from skin and subcutaneous tissue was identified as Conidiobolus incongruus.

Studies on rosette formation of human lymphocytes with pig red blood cells.

In this paper, data are presented which indicate that receptors of human peripheral blood lymphocytes (PBL) for pig erythrocytes (PRBC) and sheep erythrocytes (SRBC) are identical or at least very similar to each other with a higher avidity of PBL for SRBC than for PRBC. As an average, 50 +/- 9% of human PBL formed PRBC rosettes (Ep), compared to 70 +/- 7% of SRBC rosettes (Es). Lymphocytes incubated with SRBC plus PRBC ('co-rosetting') formed 10 +/- 5% of mixed rosettes (Em) but no pure Ep. Resuspension of rosetted lymphocytes followed by co-rosetting with the other erythrocyte species revealed that the majority of Ep became Em, while the majority of Es remained pure Es even after co-rosetting with PRCB; no pure Ep was newly formed. Incubation at 37 degrees C abolished almost all Ep as compared to 9% Es. Anti-thymocyte serum inhibited both types of rosette formation. PBL from patients with chronic lymphatic leukemia formed only 2.5 +/- 2.5% Ep. 1.7 +/- 1.1% of PBL expressed both membranes immunoglobulins and receptors for PRBC. Trypsin treatment abolished both kinds of rosette formation almost completely, while neuraminidase treatment of erythrocytes led to a raise in Ep formation from a mean of 53% to a mean percentage of 68%. Electron microscopic investigations did not reveal differences between binding sites of lymphocytes for PRCB and those for SRBC; however, with a technique different from the conventional one, intimate contact areas were observed between lymphocytes and both kinds of red blood cells.

The incidence of HLA antigens in leprosy.

HLA antigens were studied in 36 patients, with leprosy, 20 cases of lepromatous and 16 cases of tuberculoid type. Eleven out of 36 (30.55%) had BW40 as compared to 9.33% of 150 controls. The frequency of BW40 in tuberculoid patients (31.25%) was not different from that in lepromatous cases (30%).

Thyrogastric autoimmune disease. Studies on the cell-mediated immune system and histocompatibility antigens.

Cell-mediated immune responses were studied in autoimmune diseases of thyrogastric type, Hashimoto's thyroiditis and autoimmune pernicious anaemia-type gastritis. Specific cell-mediated immunity was investigated by the leucocyte migration inhibition procedure, and general cell-mediated immunity (T-cell performance) was studied by standard in vivo and in vitro tests. In thyrogastric autoimmune diseases inhibition of migration of leucocytes was induced by thyroglobulin and gastric parietal cell microsomes; under conditions of presumably low cellular sensitization, stimulation of migration was observed. There was no depression of general cell-mediated immunity, in contrast to what occurs in systemic lupus erythematosus and related autoimmune diseases. A weak association of autoimmune gastritis with HL-A3 and HL-A7 (P LESS THAN 0.05) lost significance when an appropriate correction was applied; this weakness with HL-A clearly does not explain the strong genetic component in thyroid and gastric autoimmunity.