thymosin and Anemia--Hemolytic--Autoimmune

Pathologic and immunologic features of the spontaneous autoimmune disease of NZB and NZB/NZW F1 (B/W) mice resemble human SLE in three major respects: formation of antibodies to nucleic acids, deposition of immune complexes containing DNA in the kidney, and earlier onset of severe disease in females. Genetic, viral, and hormonal factors are involved in a pathogenetic mechanism that is manifest primarily as a disturbance in immunologic regulation. Recent studies on the sequential development of IgM and then IgG antibodies to DNA and RNA suggest that the thymus, spleen, and gonads exert important regulatory influences. We have found that sex hormones modulate the expression of autoimmunity in B/W mice, with androgens suppressing and estrogens accelerating disease. The hormones may act by restoring immunologic control.

Topics: Androgens; Anemia, Hemolytic, Autoimmune; Animals; Animals, Newborn; Antibody Formation; Antigen-Antibody Complex; Autoimmune Diseases; Castration; Disease Models, Animal; DNA; Female; Gonads; Immune Tolerance; Immunity, Cellular; Immunoglobulin G; Immunoglobulin M; Lupus Erythematosus, Systemic; Male; Mice; Mice, Inbred NZB; RNA; Sex Factors; Spleen; T-Lymphocytes; Thymosin; Thymus Gland

This report describes two children in whom autoimmune hemolytic anemia was the initial clinical manifestation of an underlying T-cell deficiency. Further investigation revealed a profound deficiency of T suppressor cells in both children as detected by monoclonal T-cell antibody (OKT8) and/or functional assays. In vitro incubation of their lymphocytes with cultured thymus epithelium or thymic factors induced T suppressor cells. In vivo treatment with cultured thymus epithelium or calf thymosin fraction 5 resulted in increased T-suppressor-cell numbers and/or function in both and possibly decreased hemolytic activity in one. These results suggest that the autoimmune process in some patients with autoimmune hemolytic anemia is associated with T-suppressor-cell deficiency and that in vivo therapy with agents that modulate T-cell function may be of therapeutic value.

Topics: Adenosine Deaminase; Anemia, Hemolytic, Autoimmune; Animals; Antibodies, Monoclonal; Cattle; Cells, Cultured; Cytotoxicity, Immunologic; Erythrocytes; Female; Humans; Infant; Lymphocyte Activation; Purine-Nucleoside Phosphorylase; Rosette Formation; T-Lymphocytes; T-Lymphocytes, Regulatory; Thymosin; Thymus Gland