Blackstock R, Hernandez N C
Department of Pediatrics, University of Oklahoma Health Sciences Center, Oklahoma City 73190.
Cell Immunol. 1988 Jun;114(1):174-87. doi: 10.1016/0008-8749(88)90264-x.
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.
我们实验室之前报道过,在新生隐球菌致死性感染过程后期会出现一种抑制细胞机制。发现一种可溶性因子可抑制腹膜巨噬细胞亚群的吞噬活性。抑制细胞被鉴定为T细胞,在产生抑制吞噬作用的淋巴因子(PIL)之前,需要用特异性抗原进行体外刺激。PIL的作用具有同种异体特异性,在给予致耐受性剂量的隐球菌和非隐球菌抗原的动物中出现。当前研究进一步对负责PIL活性的T淋巴细胞进行了特征描述。发现抑制细胞处于环磷酰胺敏感途径。当用抗I-J和补体或抗Lyt-2和补体处理脾细胞群体时,未检测到PIL活性。同样,抗I-J处理细胞和抗Lyt-2处理细胞的混合物也无法合成淋巴因子。用抗Lyt-1.2或抗L3T4和补体处理脾细胞并未消除PIL的合成。对与PIL-巨噬细胞相互作用相关的遗传限制的进一步分析揭示,其受主要组织相容性复合体的I-J亚区调控。