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The past year's literature shows that little progress has been achieved in the laboratory diagnosis of autoimmune hemolytic anemia. The direct antiglobulin test is the only diagnostic test for autoimmune hemolytic anemia. Advantages of new techniques, such as the gel test, have to be determined. Today, cephalosporins are known to cause both drug-dependent and -independent autoantibodies. The diagnosis of idiopathic thrombocytopenic purpura is a clinical one. The new assays that measure antibodies against specific glycoproteins offer improved specificity. New laboratory advancements and accumulation of data on granulocytes' antigens and antibodies enabled us to recommend guidelines for the laboratory investigation of autoimmune neutropenia.

The relationship between expression of xenotropic virus and the development of autoimmunization was studied in the progeny of crosses between New Zealand Black (NZB) and SWR mice. The (F1 X SWR) and F2 progeny segregated into three phenotypes: high-virus, low-virus, and virus-negative; F1 and (F1 X NZB) progeny were always high-virus. Autoantibodies, immune deposit nephritis and lymphomas developed in the progeny of these crosses. The virological phenotype of the animal could be dissociated from the presence of either autoantibodies or nephritis. For example, mice that expressed titers of virus as high as the NZB parent failed to develop signs of autoimmunization, even up to 24 mo of age. By contrast, some (F1 X SWR) and F2 mice that expressed low titers of virus developed autoimmune disease. Furthermore, a proportion of virus-negative mice produced autoantibodies and were found to have typical immune deposit nephritis. No viral antigens could be detected in the renal lesions of such virus-negative animals. By contrast with the dissociation between expression of virus and occurrence of nephritis, the presence of antibodies to DNA correlated with the development of renal lesions. We conclude that the genes that determine the expression of infectious xenotropic virus in NZB mice segregate independently from those that are involved in the autoimmune disease of these animals.

The retroviral envelope glycoprotein, gp70 was measured in the serum of New Zealand Black (NZB) and SWR mice and the progeny of their crosses. The serum gp70 values segregated to "NZB-like" and "SWR-like" levels in these mice. A complex mechanism determined the inheritance of NZB-like serum gp70 levels. We found that the factors determining the expression of this retroviral protein were independent of the genes (Nzv-1 and Nzv-2) that determined the expression of infectious xenotropic virus. Autoimmune disease, including immune deposit nephritis could be dissociated from the degree of expression of serum gp70. By contrast, presence of circulating immune complexes and anti-DNA antibody did correlate with the development of nephritis in these crosses. A significant correlation was found between high grade expression of serum gp70 and the presence of lymphomas in these mice.