Nakayama E, Dippold W, Shiku H, Oettgen H F, Old L J
Proc Natl Acad Sci U S A. 1980 May;77(5):2890-4. doi: 10.1073/pnas.77.5.2890.
Cytotoxic T cells of the mouse express Lyt-1 as well as Lyt-2 and -3 on their surface, and T-cell cytotoxicity can be blocked by Lyt-2 and Lyt-3 (but not Lyt-1) antisera in the absence of added complement [Nakayama, E., Shiku, H., Stockert, E., Oettgen, H. F. & Old, L. J. (1979) Proc. Natl. Acad. Sci. USA 76, 1977-1981]. This analysis has now been extended to the study of the Lyt phenotype of T cells responding to alloantigens, concanavalin A (Con A), and phytohemagglutinin (PHA) and the effect of Lyt antibody on T-cell proliferation and the generation of H-2-specific killer T cells. H-2 (D/K and I), Con A, and PHA stimulation was abolished by pretreating responding cell populations with Lyt-1 antiserum and complement. Pretreatment with Lyt-2 or -3 antiserum and complement did not decrease alloantigen or Con A stimulation but did abolish PHA stimulation. Cytotoxic cells were not generated in H-2 alloantigen-primed cultures pretreated with Lyt-1, -2, or -3 antiserum and complement. When responding cells were cultured with Lyt antiserum in the absence of added complement, Lyt-2 or -3 antiserum (but not Lyt-1 antiserum) blocked alloantigen-induced proliferation and delayed generation of killer cells. Under similar conditions, Con A and PHA stimulation was not blocked by Lyt-1,-2, or -3 antiserum. Evidence from these Lyt elimination and blocking tests and from direct Lyt phenotyping of responding cells leads to the following conclusions. Two populations of Lyt(+) cells are involved: Lyt-1(+)2(-)3(-) and Lyt-1(+)2(+)3(+). Current evidence does not favor the existence of Lyt-1(-)2(+)3(+) cells but indicates that pre-killer and killer cells derive from the Lyt-1(+)2(+)3(+) population and have a Lyt-1(+)2(+)3(+) phenotype. H-2 (D/K and I) and PHA stimulation ordinarily activate the Lyt-1(+)2(+)3(+) population, whereas Con A and I region or Mls locus antigens activate the Lyt-1(+)2(-)3(-) population. However, when Lyt-1(+)2(+)3(+) cells are eliminated or blocked by Lyt-2 or -3 antiserum, H-2 alloantigen stimulation leads to proliferation of the Lyt-1(+)2(-)3(-) population. Blocking of H-2-induced proliferation by Lyt-2 or -3 antiserum adds further support to the possibility that molecules bearing Lyt-2 and -3 determinants are involved in T-cell recognition.
小鼠的细胞毒性T细胞在其表面表达Lyt-1以及Lyt-2和Lyt-3，并且在没有添加补体的情况下，T细胞的细胞毒性可被Lyt-2和Lyt-3（但不是Lyt-1）抗血清阻断[中山英、志久博、斯托克特、奥伊特根、H.F.和奥尔德、L.J.（1979年）《美国国家科学院院刊》76，1977 - 1981]。现在，这项分析已扩展到对响应同种异体抗原、刀豆球蛋白A（Con A）和植物血凝素（PHA）的T细胞的Lyt表型的研究，以及Lyt抗体对T细胞增殖和H - 2特异性杀伤性T细胞生成的影响。用Lyt-1抗血清和补体预处理响应细胞群体可消除H - 2（D/K和I）、Con A和PHA刺激。用Lyt-2或Lyt-3抗血清和补体预处理不会降低同种异体抗原或Con A刺激，但会消除PHA刺激。在用Lyt-1、Lyt-2或Lyt-3抗血清和补体预处理的H - 2同种异体抗原致敏培养物中未产生细胞毒性细胞。当响应细胞在没有添加补体的情况下与Lyt抗血清一起培养时，Lyt-2或Lyt-3抗血清（但不是Lyt-1抗血清）可阻断同种异体抗原诱导的增殖并延迟杀伤细胞的生成。在类似条件下，Con A和PHA刺激不会被Lyt-1、Lyt-2或Lyt-3抗血清阻断。这些Lyt消除和阻断试验以及响应细胞的直接Lyt表型分析的证据得出以下结论。涉及两类Lyt(+)细胞群体：Lyt-1(+)2(-)3(-)和Lyt-1(+)2(+)3(+)。目前的证据不支持Lyt-1(-)2(+)3(+)细胞的存在，但表明前杀伤细胞和杀伤细胞源自Lyt-1(+)2(+)3(+)群体并且具有Lyt-1(+)2(+)3(+)表型。H - 2（D/K和I）和PHA刺激通常激活Lyt-1(+)2(+)3(+)群体，而Con A以及I区或Mls基因座抗原激活Lyt-1(+)2(-)3(-)群体。然而，当Lyt-1(+)2(+)3(+)细胞被Lyt-2或Lyt-3抗血清消除或阻断时，H - 2同种异体抗原刺激会导致Lyt-1(+)2(-)3(-)群体增殖。Lyt-2或Lyt-3抗血清对H - 2诱导的增殖的阻断进一步支持了携带Lyt-2和Lyt-3决定簇的分子参与T细胞识别的可能性。
