Ptak W, Bereta M, Ptak M, Askenase P W
J Immunol. 1986 Mar 1;136(5):1564-70.
Recognition that delayed-type hypersensitivity (DTH) reactions, such as contact sensitivity (CS) in mice, are initiated by Ly-1+ T cell-derived, antigen-specific factors has led to identification of a new kind of suppressor T cell that regulates this initiation phase of CS. Regulation by these suppressor T cells is T cell isotype-like in that initiation of DTH of various antigenic specificities is suppressed, whereas, Ly-1+ T cells mediating the antigen/major histocompatibility complex-restricted, classic delayed phase of CS responses are not affected, nor are other T cell activities. This study shows that these isotype-specific suppressor T cells probably act by release of soluble, isotype-specific, suppressor factors. These isotype-specific T cell factors bind to and can be eluted from columns linked with antigen-specific Ly-1+ T cell factors that initiate CS, and are of different antigen specificities. These T cell regulating, anti-isotypic suppressor factors are derived from Lyt-2+ I-J- T cells and suppress CS-initiating T cells, but do not affect the delayed-acting T cells of CS. This is in contrast with antigen-specific T cell suppressor factors that affect the late-acting and not the early-acting T cells of CS. It is suggested that the antigen-binding, CS-initiating, T cell factors, and their regulatory, anti-isotypic T cell factors are, respectively, T cell analogues of immunoglobulin(Ig)E antibody, and IgE-binding factors, that regulate IgE antibody production by IgE+ B cells.
认识到迟发型超敏反应(DTH),如小鼠中的接触敏感性(CS),是由Ly-1 + T细胞衍生的抗原特异性因子引发的,这导致了一种新型抑制性T细胞的鉴定,该细胞调节CS的起始阶段。这些抑制性T细胞的调节作用类似于T细胞同种型,即各种抗原特异性的DTH起始受到抑制,而介导抗原/主要组织相容性复合体限制的CS反应经典迟发阶段的Ly-1 + T细胞不受影响,其他T细胞活性也不受影响。本研究表明,这些同种型特异性抑制性T细胞可能通过释放可溶性、同种型特异性抑制因子发挥作用。这些同种型特异性T细胞因子与引发CS的抗原特异性Ly-1 + T细胞因子连接的柱结合并可从柱上洗脱,且具有不同的抗原特异性。这些调节T细胞的抗同种型抑制因子来源于Lyt-2 + I-J- T细胞,可抑制CS起始T细胞,但不影响CS的迟发型T细胞。这与影响CS晚期作用而非早期作用T细胞的抗原特异性T细胞抑制因子形成对比。有人提出,抗原结合、引发CS的T细胞因子及其调节性抗同种型T细胞因子分别是免疫球蛋白(Ig)E抗体和IgE结合因子的T细胞类似物,它们调节IgE + B细胞产生IgE抗体。