It has recently been described that monoclonal antibody OKT 3, that reacts with the T3 determinant on all peripheral T lymphocytes in man, is also mitogenic for T cells. We have produced two monoclonal antibodies (WT 31 and WT 32) which apparently react with the T3 antigen. We have now tested the mitogenic effect of these antibodies and compared it with the mitogenicity of three other anti-T3 monoclonal antibodies, OKT 3, UCHT 1 (ref. 4) and anti-Leu 4 (ref. 5). Two distinct patterns were observed. WT 32 and OKT 3, both of the IgG2a subclass, were mitogenic for human T cells in all cases studied. By contrast, WT 31, UCHT 1 and anti-Leu 4, all of the IgG1 subclass, were devoid of mitogenic effect in 30% of the individuals tested (non-responders). The mitogenicity of all five anti-T3 antibodies was fully dependent on the presence of monocytes. Addition of purified monocytes from a responder to purified lymphocytes from a non-responder induced responsiveness to both IgG1 and IgG2a anti-T3 antibodies. These results suggest that the polymorphism in the mitogenic effect of these IgG1 antibodies is caused by polymorphism in monocyte function, possibly at the level of the Fc receptor that reacts with mouse IgG1.

Disease course and HLA antigens were determined in 29 patients with definite and 13 patients with probable adult-onset Still's disease (AOSD). Twenty-six patients had persistent disease with continuous disease activity for at least 1 year. Radiographic examination revealed evidence of joint destruction in 26 patients. In 15 patients, at least 1 root joint was impaired. The frequency of DR4 was increased in the total group of patients (35%, P = 0.03) and in the 29 patients with definite AOSD (41%, P = 0.02) compared with the frequency in normal controls (20%). None of the patients was positive for DR1, and only l was positive for Bw35. The frequency of DRw6 was increased in the patients with involvement of at least 1 root joint (40%,

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39 patients with chronic-progressive multiple sclerosis were treated with a short course of intensive immunosuppression in high doses of cyclophosphamide and prednisone. The follow-up period varied between 1 and 5 years with a mean of 21/2 years. Progression of the disease ceased in 27 patients for varying periods, with a mean of two years. In 13 patients the progression ceased during the whole follow-up period. The treatment gave the most favourable results in patients who were DRw2 positive in histocompatibility testing, whose disease started at an early age (around 28 years), whose disease duration before treatment was short (6 years), whose progression was fast and whose disability before treatment was low. If CSF levels of IgG3 months after the treatment remain low, this is a sign of good prognosis.

Frequencies of HLA-DR, Dw and DPw specificities were compared between rheumatoid arthritis (RA) patients, Felty's syndrome (FS) patients and normal controls. It was confirmed that the frequency of DR4 was increased in RA patients (54% (n = 111) vs 23% (n = 272), relative risk (RR) = 3.98, P less than 0.001). Cellular typing showed a highly significant increase in HLA-Dw14 in the entire RA population (17% (n = 32) vs 2% (n = 242), RR = 11.90, P less than 0.001), and a tendency towards an increase of HLA-Dw14 in DR4+ RA patients compared to DR4+ controls (28% (n = 32) vs 11% (n = 47), RR = 3.29, P less than 0.05). Regarding DPw specificities, the only significance was for a negative association with DPw3 (13% vs 22% (n = 254), RR = 0.51, P less than 0.05), with an additional tendential decrease of DPw1 (11% vs 19%, RR = 0.53, not significant (NS]. The decrease of DPw3 was more marked in DR4- RA patients (RR = 0.33, P less than 0.05) than in DR4+ RA patients (RR = 0.69, NS). In FS patients, 96% of whom were DR4+, decreased DPw1 was very marked, whereas the frequency of DPw3 was unaltered compared to DR4+ normals. These alterations in frequencies were not caused by linkage disequilibria between HLA-DR and -DP alleles. Thus, taken together, these data suggest that, in the presence of the major DR4-associated "susceptibility" gene(s) for RA, DPw1 may have "protective" effects, whereas in the absence of DR4, the presence of DPw3 has significant "protective" activity.