Our laboratory has previously reported a suppressor cell mechanism to occur late in the course of a lethal infection with Cryptococcus neoformans. A soluble factor was found to be responsible for inhibition of the phagocytic activity of a subpopulation of peritoneal macrophages. The suppressor cell was identified as a T cell which required in vitro stimulation with specific antigen before the phagocytosis-inhibiting lymphokine (PIL) was produced. PIL action was allospecific and occurred in animals given tolerogenic doses of cryptococcal and noncryptococcal antigens. The current investigation has further characterized the T lymphocyte responsible for PIL activity. The suppressor cell was found to be in a cyclophosphamide-sensitive pathway. PIL activity was not detected when spleen cell populations were treated with anti-I-J and complement or anti-Lyt-2 and complement. Likewise, a mixture of anti-I-J-treated and anti-Lyt-2-treated cells was incapable of synthesizing the lymphokine. Treatment of spleen cells with anti-Lyt-1.2 or anti-L3T4 and complement did not eliminate PIL synthesis. Further analysis of the genetic restrictions associated with the PIL-macrophage interaction revealed regulation by the I-J subregion of the major histocompatibility complex.
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