Alloantigen-induced T-cell proliferation: Lyt phenotype of responding cells and blocking of proliferation by Lyt antisera.
Alloantigen-induced T-cell proliferation: Lyt phenotype of responding cells and blocking of proliferation by Lyt antisera.
复制标题
同种抗原诱导的 T 细胞增殖：响应细胞的 Lyt 表型以及 Lyt 抗血清对增殖的阻断。
DOI：
10.1073/pnas.77.5.2890
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发表时间：
1980
影响因子：
11.1
通讯作者：
L. Old
中科院分区：
文献类型：
--
作者：
E. Nakayama;W. Dippold;H. Shiku;H. Oettgen;L. Old
小鼠的细胞毒性T细胞在其表面表达Lyt-1以及Lyt-2和-3，并且在没有添加补体的情况下，T细胞的细胞毒性可以被Lyt-2和Lyt-3（但不能被Lyt-1）抗血清阻断[Nakayama， E., Shiku， H., Stockert， E., Oettgen， H. F. & Old， L. J. (1979) Proc. Natl。学会科学。《美国科学》第76期，1977-1981。这种分析现在已经扩展到T细胞对异体抗原、豆豆蛋白A （Con A）和植物血凝素（PHA）反应的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T细胞产生的影响。用Lyt-1抗血清和补体预处理应答细胞群，可消除H-2 （D/K和I）、Con A和PHA的刺激。Lyt-2或-3抗血清和补体预处理不能减少同种异体抗原或Con A刺激，但可以消除PHA刺激。用Lyt-1、-2或-3抗血清和补体预处理的H-2异体抗原引物培养物中不产生细胞毒性细胞。当应答细胞在不添加补体的情况下用Lyt抗血清培养时，Lyt-2或-3抗血清（而不是Lyt-1抗血清）阻断了同种异体抗原诱导的增殖并延迟了杀伤细胞的产生。在类似条件下，Lyt-1、-2或-3抗血清不阻断Con A和PHA的刺激。来自这些Lyt消除和阻断试验的证据以及来自应答细胞的直接Lyt表型的证据导致以下结论。Lyt（+）细胞涉及两个群体：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来源于Lyt-1(+)2(+)3（+）群体，并具有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和I区或Mls位点抗原激活Lyt-1(+)2(-)3（-）群体。然而，当Lyt-1(+)2(+)3（+）细胞被Lyt-2或-3抗血清消除或阻断时，H-2同种异体抗原刺激导致Lyt-1(+)2(-)3（-）细胞增殖。Lyt-2或-3抗血清阻断h -2诱导的增殖进一步支持了携带Lyt-2和-3决定因子的分子参与t细胞识别的可能性。
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.