AIDS and lymphadenopathy syndrome (LAS) patients display similar abnormal in vitro proliferation and differentiation of T-colony forming cells (T-CFC).

T-cell colonies were generated from the peripheral blood and bone marrow of 61 patients with acquired immunodeficiency syndrome (AIDS), 54 patients with persistent lymphadenopathy syndrome (LAS), 14 clinically normal male homosexuals, and 17 healthy heterosexuals. Mononuclear cells were cultured in methylcellulose in the presence of IL2-containing conditioned medium. The number of T-cell forming cells (T-CFC) from healthy male homosexuals and AIDS and LAS patients was significantly (P less than 0.01) reduced compared to T-CFC from healthy heterosexuals. In AIDS patients, the low colony growth capacity of T-CFC was independent of the presence of either opportunistic infections or Kaposi sarcoma. Twelve LAS patients who subsequently developed AIDS showed the lowest capacity of peripheral blood and bone marrow T-CFC to proliferate. Pooled induced colonies from AIDS and LAS patients and normal homosexuals were composed of immature cells bearing the T3+, T4+, T6+, and T8+ surface phenotype, unlike colonies from normal heterosexuals, which displayed mature cells bearing the T3+, T4+, T6-, and T3+, T8+, T6- surface phenotype. Moreover, most T-CFC from primary colonies had lost their self-renewal capacity. In some AIDS and LAS patients but not healthy homosexuals peripheral blood and bone marrow T-CFC were capable of generating colonies with recombinant IL2 (rIL2) without any other mitogenic stimulation. The rIL2-induced colony growth was abrogated by a monoclonal antibody against the IL2 receptor. These results suggest that early impairment of T-CFC plays a predominant role in the pathogenesis of AIDS.