Murphy J W
Infect Immun. 1985 May;48(2):439-45. doi: 10.1128/iai.48.2.439-445.1985.
Cell-mediated immunity is an important aspect of host resistance against Cryptococcus neoformans. Using a CBA/J murine model, we demonstrated that injection of cryptococcal antigen (CneF) at dosages sufficient to stimulate the antigenemia observed in cryptococcosis patients induces specific T-cell-mediated suppression of the cryptococcal delayed-type hypersensitivity response. The purpose of this study was to establish whether Lyt 1+, first-order T-suppressor (Ts1) cells block the induction of T cells responsible for delayed-type hypersensitivity (TDH cells) or whether they function by inducing Lyt 2+, efferent suppressor (Ts2) cells. In one set of experiments, suppression was observed when Ts1 cells were adoptively transferred to recipient animals the day before, the day of, or the day after immunization; however, when Ts1 cells were transferred after TDH cells were present, no suppression occurred. In other experiments, putative TDH cells from lymph nodes (LN) or spleens were adoptively transferred from mice after immunization or after a suppressive dose of CneF or adoptive transfer of Ts1 cells and immunization. Delayed-type hypersensitivity could not be transferred with LN or spleen cells from mice receiving the suppressive dose of CneF or the Ts1 cells, even when the LN or spleen cells were treated with anti-Lyt 2.1 antibody and complement to remove any Ts2 cells. Delayed-type hypersensitivity was readily transferred with LN or spleen cells from immunized mice whether the cells were or were not treated with anti-Lyt 2 and complement. Furthermore, the cells in the tolerized LN cell pools responsible for suppression of TDH cell induction were Lyt 1+ 2-, I-J+ cells, which is the phenotype of the Ts1 cells. Taken together, these data indicate that Ts1 cells inhibit the induction of TDH cells. This finding, coupled with the previous demonstration that Ts1 cells or a Ts1 cell-derived soluble factor (TsF1) induces Ts2 cells, establishes that the cryptococcal Ts1 cells are bifunctional in the suppressive pathway.
细胞介导的免疫是宿主抵抗新型隐球菌的一个重要方面。利用CBA/J小鼠模型，我们证明，以足以刺激隐球菌病患者体内观察到的抗原血症的剂量注射隐球菌抗原（CneF），可诱导特异性T细胞介导的对隐球菌迟发型超敏反应的抑制。本研究的目的是确定Lyt 1 +一级T抑制细胞（Ts1细胞）是阻断负责迟发型超敏反应的T细胞（TDH细胞）的诱导，还是通过诱导Lyt 2 +传出抑制细胞（Ts2细胞）发挥作用。在一组实验中，当在免疫前一天、免疫当天或免疫后一天将Ts1细胞过继转移至受体动物时，观察到了抑制作用；然而，当在TDH细胞出现后转移Ts1细胞时，则未发生抑制作用。在其他实验中，在免疫后、给予抑制剂量的CneF后或过继转移Ts1细胞并免疫后，从小鼠的淋巴结（LN）或脾脏中过继转移假定的TDH细胞。即使在用抗Lyt 2.1抗体和补体处理以去除任何Ts2细胞后，接受抑制剂量的CneF或Ts1细胞的小鼠的LN或脾细胞也无法转移迟发型超敏反应。无论是否用抗Lyt 2和补体处理，来自免疫小鼠的LN或脾细胞都很容易转移迟发型超敏反应。此外，负责抑制TDH细胞诱导的耐受LN细胞池中的细胞是Lyt 1 + 2 -、I-J +细胞，这是Ts1细胞的表型。综上所述，这些数据表明Ts1细胞抑制TDH细胞的诱导。这一发现，再加上之前证明Ts1细胞或Ts1细胞衍生的可溶性因子（TsF1）可诱导Ts2细胞，证实隐球菌Ts1细胞在抑制途径中具有双重功能。
