Flood P, Ptak W, Green D R
J Immunol. 1986 Sep 15;137(6):1829-35.
The passive transfer of contact sensitivity (CS) by immune cells into normal animals requires the interaction of two distinct Ly-1+ T cells, one which is Vicia villosa lectin (VV)-nonadherent, the other which adheres to VV. Functional deletion of either cell type abrogates the adoptive transfer of CS into normal animals, whereas VV-nonadherent cells alone can transfer CS into animals pretreated with cyclophosphamide (Cy). An antigen-specific T suppressor factor, designated TNP-TsF, inhibits the transfer of CS into normal adoptive recipients. TNP-TsF mediates its suppressive activity by inducing an I-J+ subfactor (designated I-J2) from the assay population by the interaction of PC1-F (a TNP-binding subfactor of TNP-TsF) with antigen-primed Ly-2+ T cells. This I-J+ subfactor then complements TNBS-F (an antigen-nonbinding subfactor of TNP-TsF) to form an antigen-nonspecific effector molecule which suppresses DTH responses in an antigen-nonspecific fashion. We report here that TNP-TsF suppresses the adoptive transfer of CS into normal animals but not into animals pretreated with Cy. TNBS-F + I-J2, the effector complex of TNP-TsF, also suppresses the transfer of CS into normal but not Cy-treated animals. When the Ly-1 immune cells were separated into VV-adherent and -nonadherent populations, the TNBS-F + I-J2 suppressor complex suppressed the functional activity of the VV-adherent cell population, but not the VV-nonadherent cells. This suppressive activity correlates with the need for VV-adherent cells in the transfer of CS into normal but not Cy-treated recipients. When an I-J+ molecule (I-J1) from an SRBC-specific TsF was used in place of I-J2 to form a suppressor complex with TNBS-F, this TNBS-F + I-J1 TsF suppressed the transfer of CS into both normal and Cy-treated recipients. This difference in functional suppressive activity correlated with a difference in target cell specificity: TNBS-F + I-J1 suppressed the VV-nonadherent TDTH cell, whereas TNBS-F + I-J2 suppressed the VV-adherent T cell of CS. Immune cells which are transferred under conditions which do not require the VV-adherent cell for transfer are not suppressed by TNBS-F + I-J2 or TNP-TsF, but are suppressed by the TNBS-F + I-J1.(ABSTRACT TRUNCATED AT 250 WORDS)
免疫细胞将接触敏感性(CS)被动转移至正常动物体内需要两种不同的Ly-1⁺ T细胞相互作用,一种是绒毛野豌豆凝集素(VV)非黏附性的,另一种是能黏附于VV的。任一种细胞类型的功能缺失都会消除CS向正常动物的过继转移,而单独的VV非黏附性细胞能将CS转移至用环磷酰胺(Cy)预处理的动物体内。一种抗原特异性T抑制因子,命名为TNP-TsF,可抑制CS向正常过继受体的转移。TNP-TsF通过PC1-F(TNP-TsF的一种TNP结合亚因子)与抗原致敏的Ly-2⁺ T细胞相互作用,从测定群体中诱导出一种I-J⁺亚因子(命名为I-J2),从而介导其抑制活性。然后这种I-J⁺亚因子与TNBS-F(TNP-TsF的一种抗原非结合亚因子)互补形成一种抗原非特异性效应分子,以抗原非特异性方式抑制迟发型超敏反应(DTH)。我们在此报告,TNP-TsF抑制CS向正常动物的过继转移,但不抑制向用Cy预处理的动物的转移。TNP-TsF的效应复合物TNBS-F + I-J2也抑制CS向正常但不向经Cy处理动物的转移。当将Ly-1免疫细胞分离为VV黏附性和非黏附性群体时,TNBS-F + I-J2抑制复合物抑制VV黏附性细胞群体的功能活性,但不抑制VV非黏附性细胞。这种抑制活性与CS向正常但非经Cy处理受体转移过程中对VV黏附性细胞的需求相关。当用来自抗绵羊红细胞特异性TsF的一种I-J⁺分子(I-J1)代替I-J2与TNBS-F形成抑制复合物时,这种TNBS-F + I-J1 TsF抑制CS向正常和经Cy处理受体的转移。这种功能抑制活性的差异与靶细胞特异性的差异相关:TNBS-F + I-J1抑制VV非黏附性迟发型超敏T细胞,而TNBS-F + I-J2抑制CS的VV黏附性T细胞。在不需要VV黏附性细胞进行转移的条件下转移的免疫细胞,不受TNBS-F + I-J2或TNP-TsF的抑制,但受TNBS-F + I-J1的抑制。(摘要截短于250字)