Using immunoblot analysis with soluble nuclear extracts from HeLa cells, we identified autoantibodies to an antigen with a molecular weight of -33,000 in 36% of 95 sera from rheumatoid arthritis patients, but in only 1 of 170 controls. The antigen, termed RA33, was resistant to DNase and RNase digestion but sensitive to proteinase K treatment. There was no discernible relation to other autoantibodies. Thus, this newly described autoantibody appears to be highly specific for rheumatoid arthritis.Anticytoplasmic and antinuclear antibodies (ANA) are common serologic findings in patients with
Annals of the Rheumatic Diseases, 35, 446-450. Demonstration of antibodies to collagen and of collagen-anticollagen immune complexes in rheumatoid arthritis synovial fluids. Twenty-nine synovial fluids from patients with rheumatoid arthritis (RA) and 10 synovial fluids from patients with other joint diseases were investigated with regard to the presence of antibodies to denatured human collagen and of collagen-anticollagen immune complexes. 12 of the 29 RA synovial fluids showed anticollagen titres from 1: 16 to 1: 512 in passive haemagglutination. Only one patient in the group with no arthritis had a significant anticollagen titre of 1: 32. Digestion of the synovial fluids with bacterial collagenase resulted in an anticollagen titre increase from two to four dilution steps in 9 of the RA fluids, while 6 previously negative RA synovial fluids showed anticollagen titres from 1: 32 to 1: 128 after digestion with collagenase. These results indicate the existence of collagen-anticollagen immune complexes in 15 of the 29 RA synovial fluids investigated.
Bronchoalveolar lavage (BAL) was performed on 70 RA patients, 28 without extra-articular manifestations, nine with pulmonary involvement, 13 with sicca-syndrome, 20 with other extra-articular manifestations such as renal involvement, cutaneous vasculitis and rheumatoid nodules. Fifteen patients without rheumatic or pulmonary disease served as the control group. Compared with the control group RA patients showed a statistically significant increase of lymphocytes, especially of activated (DR+)T(CD3+)-helper (CD4+) cells, resulting in a significantly diminished percentage of alveolar macrophages, B(CD21+)-lymphocytes, T-suppressor (CD8+) cells and an increased CD4/CD8 ratio. This cell distribution pattern was more pronounced in RA patients with lung involvement with significant differences to the other RA patients with regard to lymphocytes, DR positive cells and CD4 positive/DR positive cells. It is concluded that these results indicate an altered balance of immunocompetent cells not only in the joints but also in the lung. The changes are more distinct if local manifestations can be diagnosed clinically.
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