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Polyclonal activation of B-lymphocytes accompanies many retroviral infections. Friend derived murine immunosuppressive virus (Fd-MIV) is a non-defective murine retrovirus which was isolated from T-helper cells from mice infected with the acute transforming retrovirus Friend leukaemia complex (FLC). In contrast to FLC, Fd-MIV does not induce acute transformation of lymphoid and erythroid cells but causes immunosuppression and lymphadenopathy in adult NMRI mice. The effect of Fd-MIV infection on B-lymphocytes was studied. Fd-MIV infection led to a persistent hypergammaglobulinemy with a significant increase in the level of circulating IgG, IgM and immune complexes. In the spleen and lymph nodes, B-lymphocyte proliferation was found. Parallel to the development of hypergammaglobulinemy, autoantibodies to a variety of nuclear and other autoantigens was detected. In conclusion, the Fd-MIV infection leads to a B-lymphocyte dysfunction that has many parallels with AIDS. Furthermore, the Fd-MIV infection seems to represent an example of an autoimmune condition caused by an exogenous infectious agent.

A Norwegian family showed 20 cases of verified or suspected diabetes in 5 generations, 13 being females and 7 males. In 12 patients the diagnosis was established at 26 years of age or earlier. Fourteen patients were definitely non-insulin-dependent. A high frequency of severe diabetic ophthalmopathy was noted, five patients were blind, two had proliferative retinopathy, and one simplex retinopathy and cataract. Five patients from the last 3 generations were islet cell antibody negative and C-peptide positive. In selected patients the serum insulin response to oral glucose was markedly reduced. HLA determinations in these patients showed absence of DR3 and DR4, and presence of DR2. The inheritance of diabetes in this family is compatible with an autosomal, dominant trait, and the majority of cases fulfilled the criteria of maturity-onset diabetes of the young. The high frequency of severe ophthalmopathy underscores that this disease may have an unfavourable evolution.

Sarcoidosis and hypersensitivity pneumonitis are diffuse parenchymal lung diseases characterized by formation of non-caseating granulomas with a bronchocentric distribution. Analysis of the white blood cell differential profile in bronchoalveolar lavage fluid can be a useful supplement in the diagnostic work-up.Diagnostic markers that can improve the discrimination of sarcoidosis and hypersensitivity pneumonitis are wanted.Bronchoalveolar lavage fluid fractions of CD4+ and CD8+ T cells expressing the activation marker HLA-DR and fractions of natural killer T cells determined by flow cytometry were investigated in sarcoidosis (N=83), hypersensitivity pneumonitis (N=10) and healthy control subjects (N=15).In hypersensitivity pneumonitis, natural killer T cell fractions were over 7-fold greater [median (IQR): 5.5% (3.5-8.1) versus 0.7% (0.5-1.2), p0.0001], and HLA-DR+ fractions of CD8+ lymphocytes were almost two fold greater [median (IQR): 79% (75-82) versus 43% (34-52), p0.0001] than in sarcoidosis. In healthy control subjects, natural killer T cell fractions of leucocytes and HLA-DR+ fractions of CD8+ lymphocytes were lower [median (IQR): 0.3% (0.3-0.6) and 30% (26-34), p=0.02 and p=0.01 compared to sarcoidosis]. The combined use of these two markers seems to discriminate the diseases very well.This study suggests a role for the bronchoalveolar lavage fluid lymphocyte subsets HLA-DR+ CD8+ T cells and natural killer T cells in the diagnostic work up of sarcoidosis and hypersensitivity pneumonitis.