Mechanisms of induction of primary virus‐specific cytotoxic T lymphocyte responses
Mechanisms of induction of primary virus‐specific cytotoxic T lymphocyte responses
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原发性病毒特异性细胞毒性 T 淋巴细胞反应的诱导机制
DOI：
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发表时间：
1992
影响因子：
5.4
通讯作者：
C. Melief
中科院分区：
文献类型：
--
作者：
M. De Bruijn;J. Nieland;T. Schumacher;H. Ploegh;W. Martin Kast;C. Melief
我们研究了各种抗原呈递细胞（APC）类型通过单一体外刺激诱导原代抗病毒细胞毒性T淋巴细胞（CTL）应答的能力。在这些APC类型中，只有树突状细胞（DC）和RMA‐S淋巴瘤细胞可以诱导初级CTL应答，但通过不同的机制。DC能够通过呈递病毒肽或经处理的感染性病毒产生原代病毒特异性CTL。与此相反，RMA‐S细胞不能呈递内源性抗原，例如：G.在病毒感染后，该细胞系非常有效地呈递外源病毒肽以在体外诱导原代病毒特异性CTL。脾细胞、脂多糖诱导的B细胞母细胞或未突变的RMA细胞不具有通过单一体外刺激触发未致敏的T细胞的能力。我们已经研究了DC和RMA-S细胞诱导初级CTL应答的几个重要特征（总结于图6）。抗LFA-1或抗CD 8单克隆抗体（mAb）阻断DC或RMA-S细胞诱导的原发性CTL应答。DC与未致敏的T细胞迅速聚集，这不依赖于LFA-1和CD 8分子。RMA-S细胞不与未引发的T细胞形成缀合物。尽管它们丰富的主要组织相容性复合物（MHC）I类细胞表面表达，DC并不结合大量外源性添加的病毒肽。相比之下，RMA‐S细胞上的MHC I类分子与大量外源性肽结合。DC的强大粘附和RMA‐S细胞上相关MHC/肽复合物的高表达是与未引发的T淋巴细胞初始接触的重要特征。在接触的后期阶段，DC和RMA-S细胞都激活T细胞表面的LFA-1（和CD 8）分子，以加强和维持T细胞与APC之间的接触。
We have investigated the ability of various antigen‐presenting cell (APC) types to induce primary anti‐viral cytotoxic T lymphocyte (CTL) responses by single in vitro stimulation. Of these APC types, only dendritic cells (DC) and RMA‐S lymphoma cells could induce primary CTL responses, but by divergent mechanisms. DC were capable of generating primary virus‐specific CTL, either by presenting viral peptide or processed infectious virus. In contrast, RMA‐S cells could not present endogenous antigen, e. g. after virus infection, but this cell line very efficiently presented exogenous viral peptides to induce primary virus‐specific CTL in vitro. Spleen cells, lipopolysaccharide‐induced B cell blasts or the non‐mutated RMA cells did not have the ability to trigger unprimed T cells by single in vitro stimulation. We have investigated several characteristics important for primary CTL response induction by DC and RMA‐S cells (summarized in Fig. 6). Primary CTL response induction by DC or RMA‐S cells was blocked by anti‐LFA‐1 or anti‐CD8 monoclonal antibodies (mAb). DC rapidly aggregated with unprimed T cells, which was independent of LFA‐1 and CD8 molecules. RMA‐S cells did not form conjugates with unprimed T cells. Despite their abundant major histocompatibility complex (MHC) class I cell‐surface expression, DC did not bind much exogenously added viral peptide. In contrast, the MHC class I molecules on RMA‐S cells bound a large quantity of exogenously administered peptide. Powerful adhesion by DC and high expression of relevant MHC/peptide complexes on RMA‐S cells are important features in the initial contact with unprimed T lymphocytes. In a later stage of contact, both DC and RMA‐S cells activate LFA‐1 (and CD8) molecules at the T cell surface to strengthen and maintain the contact between T cell and APC.
同种异体抗原识别之前是细胞毒性 T 细胞和靶细胞的非特异性粘附。
DOI：
10.1126/science.3485822
发表时间：
1986
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Spits,H;vanSchooten,W;Keizer,H;vanSeventer,G;vandeRijn,M;Terhorst,C;deVries,JE
通讯作者：
deVries,JE
用 H-2 突变体分析对仙台病毒的细胞毒性 T 淋巴细胞反应的调节。
DOI：
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发表时间：
1983
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
deWaal,LP;Kast,WM;Melvold,RW;Melief,CJ
通讯作者：
Melief,CJ