Wang Z Q, Bapat A S, Trejo V, Orlikowsky T, Mittler R S, Hoffmann M K
Department of Microbiology and Immunology, New York Medical College, Valhalla, New York, 10595, USA.
Cell Immunol. 1999 Apr 10;193(1):108-14. doi: 10.1006/cimm.1999.1454.
Three T cell populations can be distinguished based on their response to antigen receptor engagement. A sizable fraction dies within hours of TCR ligation, a smaller fraction enters the mitotic cycle, and the remaining T cells merely upregulate the expression of certain cell surface markers. An MHC-I-controlled regulatory mechanism has been identified. MHC I MAbs, or Fab fragments, prevent T cells from mounting a proliferative mitogen response but do not inhibit the mitogen-induced deletion of T cells. IFN-gamma enlarges the fraction of T cells which proliferate in response to mitogen stimulation but, in the presence of MHC I MAb, these cells fail to clonally expand and enter the deletion pathway. Phenotypically, MHC I MAb Fab fragments induce T cells to upregulate the expression of the apoptosis marker CD95, even in the absence of TCR ligand, and prevent the upregulation of costimulatory CD28 molecule expression.
根据对抗原受体结合的反应，可以区分出三种T细胞群体。相当一部分T细胞在TCR连接后的数小时内死亡，一小部分进入有丝分裂周期，其余的T细胞仅仅上调某些细胞表面标志物的表达。一种由MHC-I控制的调节机制已被确定。MHC I单克隆抗体或Fab片段可阻止T细胞产生增殖性丝裂原反应，但不抑制丝裂原诱导的T细胞缺失。干扰素-γ增加了对丝裂原刺激产生增殖反应的T细胞比例，但是，在存在MHC I单克隆抗体的情况下，这些细胞无法进行克隆性扩增并进入缺失途径。从表型上看，MHC I单克隆抗体Fab片段即使在没有TCR配体的情况下也能诱导T细胞上调凋亡标志物CD95的表达，并阻止共刺激分子CD28表达的上调。
