Morse H C, Yetter R A, Via C S, Hardy R R, Cerny A, Hayakawa K, Hugin A W, Miller M W, Holmes K L, Shearer G M
Laboratory of Immunopathology, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892.
J Immunol. 1989 Aug 1;143(3):844-50.
The functional and phenotypic characteristics of Ly-4(CD4)+ and Ly-2(CD8)+ T cells were studied after induction of murine AIDS with LP-BM5 murine leukemia virus. Assays of spleen cells for their ability to generate in vitro CTL responses to TNP-modified autologous cells (self + x CTL) and to alloantigens (allo CTL) showed that self + x CTL responses were greatly impaired at 3 to 4 wk postinfection and were undetectable thereafter. Allo CTL responses were normal at 3 to 4 wk, but were reduced at 8 to 9 wk and absent at 14 wk postinfection. This sequential loss of self + x and allo CTL responses was related to a selective defect in Ly-4(CD4)+ Th cell function associated with impaired production of IL-2 and deficient proliferative responses to Con A or to soluble Ag. Changes in the functional characteristics of Ly-4(CD4)+ T cells were unrelated to changes in their frequency in spleen, but did correlate with marked alterations in their distribution among four subsets defined by mAb SM3C11 and SM6C10. Assays of CTL responses generated by mixtures of spleen cells from normal and infected mice suggested that active suppression of Ly-4(CD4)+ Th function may contribute to this defect. Studies of Ly-2(CD8)+ T cells showed that infection with LP-BM5 murine leukemia virus also induced a major phenotypic shift in subpopulations defined by their reactivity with mAb 6C10. However, this phenotypic change did not appear to correlate with major functional defects.
用LP - BM5鼠白血病病毒诱导小鼠患艾滋病后，研究了Ly - 4(CD4)+和Ly - 2(CD8)+ T细胞的功能和表型特征。检测脾细胞对TNP修饰的自体细胞（自身+x CTL）和同种抗原（同种异体CTL）产生体外CTL反应的能力，结果显示，感染后3至4周，自身+x CTL反应严重受损，此后无法检测到。同种异体CTL反应在感染后3至4周正常，但在8至9周时降低，在14周时消失。自身+x和同种异体CTL反应的这种相继丧失与Ly - 4(CD4)+ Th细胞功能的选择性缺陷有关，该缺陷与IL - 2产生受损以及对Con A或可溶性抗原的增殖反应不足有关。Ly - 4(CD4)+ T细胞功能特征的变化与其在脾脏中的频率变化无关，但与它们在由单克隆抗体SM3C11和SM6C10定义的四个亚群中的分布的显著改变相关。对正常小鼠和感染小鼠的脾细胞混合物产生的CTL反应的检测表明，Ly - 4(CD4)+ Th功能的主动抑制可能导致了这种缺陷。对Ly - 2(CD8)+ T细胞的研究表明，感染LP - BM5鼠白血病病毒也诱导了由其与单克隆抗体6C10反应性定义的亚群中的主要表型转变。然而，这种表型变化似乎与主要的功能缺陷无关。
