02510nas a2200349 4500000000100000008004100001260001300042653002200055653004100077653001100118653002100129653001200150653002000162653003100182653002700213653002900240653002500269653001800294653005700312100002200369700001400391700001900405700002600424700001400450700001300464700002100477245012000498300001000618490000700628520151100635022001402146 1987 d c1987 Dec10aAntigens, Surface10aHistocompatibility Antigens Class II10aHumans10aInterferon-gamma10aleprosy10aLeukocyte Count10aReceptors, Antigen, T-Cell10aReceptors, Immunologic10aReceptors, Interleukin-210aRecombinant Proteins10aT-Lymphocytes10aTumor Necrosis Factor Receptor Superfamily, Member 71 aGonzález-Amaro R1 aBaranda L1 aAbud-Mendoza C1 aSalazar-González J F1 aMoncada B1 aGarcia R1 aAlcocer-Varela J00aQuantitative analysis of contrasuppressor T lymphocytes in leprosy; induction of Ia antigens with gamma interferon. a651-60 v553 a

Lepromatous leprosy is characterized by immune anergy and abnormal suppressor T-cell function. Contrasuppressor cells are a subset of CD8+, vicia villosa-adherent T lymphocytes. T-contrasuppressor (Tcs) cells act on T-helper cells to cause them to become unresponsive to the action of T-suppressor cells. In 8 lepromatous (LL) and 7 tuberculoid (TT) patients, and 6 healthy contacts we studied the percent of the following lymphocyte subsets: CD3+, CD4+, CD8+, Ia+, vicia villosa+ (VV+), CD8, VV+, VV, Ia+, and Ia, Tac+. This was done in baseline status as well as post-stimulation with recombinant gamma interferon (rIFN-gamma). We found that peripheral blood mononuclear cells from LL and TT patients and controls exhibit a similar number of putative contrasuppressor lymphocytes (CD8, VV+ cells). However, in the contrasuppressor subset from LL patients we found a low percent of Ia+ (p less than 0.05 compared to controls or TT). In the three groups studied, the rIFN-gamma enhanced the percent of Ia+ lymphocytes in the CD8, VV+ cell subpopulation. However, the CD8, VV+ lymphocytes from LL patients, despite the effect of rIFN-gamma, continue to have a low percent of Ia+ cells (p less than 0.05 compared to controls or TT). These findings suggest that LL patients might have abnormalities in the contrasuppressor immune circuit. Future functional studies on the role of Tcs cells in the anergy seen in LL will be required in order to define the apparent dysfunction occurring in this disease.

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