Taylor C E, Fauntleroy M B, Stashak P W, Baker P J
Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, Rockville, Maryland 20852.
Infect Immun. 1991 Feb;59(2):575-9. doi: 10.1128/iai.59.2.575-579.1991.
Previous studies have shown that transfer of whole spleen cell populations obtained from primed donors or transfer of purified T cells enriched for suppressor activity (Ts) to recipient mice decreased the antibody response to pneumococcal polysaccharide type III (SSS-III) when the animals were simultaneously immunized with SSS-III. In the present studies, such suppression of the antibody response was transferred with 10- to 100-fold fewer primed spleen cells when the cells were treated in vitro with recombinant interleukin-2 (rIL-2) before transfer; spleen cells from naive mice or mice primed with an unrelated antigen (dextran) and then treated with rIL-2 did not cause suppression of the antibody response to SSS-III, thereby eliminating the possibility of nonspecific carryover effects induced by rIL-2. In vivo administration of rIL-2 at the time of immunization with an optimally immunogenic dose of SSS-III resulted in significant (P less than 0.05) suppression of the antibody response relative to that of control animals, suggesting that IL-2 augments the clonal expansion of Ts cells in vivo. Further, the ability of passively administered anti-IL-2 receptor antibody to inhibit generation of Ts cells in vivo is consistent with such a view. Spleen cells from primed animals treated with rIL-4, rIL-5, or gamma interferon--but not those from primed animals treated with rIL-6--likewise were able to transfer suppression of the antibody response with fewer cells than those required when primed cells not treated with lymphokines were used. Thus, these studies indicate that Ts cell activity is greatly influenced by lymphokines produced by helper T cells. The studies also suggest that these lymphokines are required during activation and/or clonal expansion of Ts cells.
先前的研究表明,当用III型肺炎球菌多糖(SSS-III)同时免疫动物时,将从致敏供体获得的全脾细胞群体进行转移,或转移富含抑制活性(Ts)的纯化T细胞至受体小鼠,会降低对SSS-III的抗体反应。在本研究中,当细胞在转移前用重组白细胞介素-2(rIL-2)进行体外处理时,用少10至100倍的致敏脾细胞就能转移这种抗体反应的抑制作用;来自未致敏小鼠或用无关抗原(葡聚糖)致敏然后用rIL-2处理的小鼠的脾细胞,不会引起对SSS-III抗体反应的抑制,从而排除了rIL-2诱导的非特异性残留效应的可能性。在用最佳免疫原剂量的SSS-III免疫时体内给予rIL-2,相对于对照动物,抗体反应受到显著(P小于0.05)抑制,这表明IL-2在体内增强了Ts细胞的克隆扩增。此外,被动给予的抗IL-2受体抗体在体内抑制Ts细胞生成的能力也与这种观点一致。用rIL-4、rIL-5或γ干扰素处理的致敏动物的脾细胞——但用rIL-6处理的致敏动物的脾细胞则不然——同样能够用比未用淋巴因子处理的致敏细胞所需细胞数更少的细胞来转移抗体反应的抑制作用。因此,这些研究表明,Ts细胞活性受到辅助性T细胞产生的淋巴因子的极大影响。这些研究还表明,这些淋巴因子在Ts细胞的激活和/或克隆扩增过程中是必需的。