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目的：皮肤Ｔ细胞淋巴瘤（ＣＴＣＬ）是记忆性诱导Ｔ细胞肿瘤，表达独特的Ｔ细胞受体（ＴＣＲ）的α和β链，两者各含有克隆性独特蛋白序列。这些序列由独特型或第３决定簇互补区（ＣＤＲ３）组成。理论上，来源于ＴＣＲＣＤＲ３的肽类可作为由主要组织相容性复合体（ＭＨＣ）Ⅰ类分子提呈的肿瘤特异抗原。本研究旨在确定细胞毒性Ｔ淋巴细胞（ＣＴＬ）是否识别ＣＤＲ３来源的肽类。方法：首先培育出能裂解２例ＣＴＣＬ病人自身的肿瘤细胞的ＣＴＬ（ＣＤ８＋）细胞株，然后检测这些ＣＴＬ对由原始Ｂ淋巴细胞提呈的源于自身恶性细胞ＴＣＲＣＤＲ３序列的合成肽产生应答的能力。结果：ＣＴＬ分泌肿瘤坏死因子（ＴＮＦα），对自身ＴＣＲβ链独特型肽产生应答，但对来源于其他ＴＣＲβ链独特型区的肽或对照肽不产生应答。抗ＭＨＣⅠ类分子的单克隆抗体（Ｗ６／３２）能阻断其肽的识别。结论：首先表明ＣＴＬ可识别具有ＣＴＣＬ病人个体独特性的恶性淋巴细胞克隆的特异ＭＨＣⅠ类分子相关肽并对其产生应答；又提示起刺激作用的肽来源于ＴＣＲβ链独特型区。该研究建立了这种机制，其他Ｔ细胞可通过此机制调解既定的抗原特异性Ｔ细胞。ＣＴＣＬ的肿瘤特异性表位的鉴定，可能有助开发强化或启动ＣＤ８介导的?
PURPOSE: Cutaneous T-cell lymphoma (CTCL) is a memory-induced T cell tumor that expresses both the alpha and beta chains of the unique T cell receptor (TCR), each containing a clonally unique protein sequence. These sequences consist of an idiotype or complementarity-determining region (CDR3). In theory, peptides derived from TCRCDR3 are tumor-specific antigens presented by class I molecules of the major histocompatibility complex (MHC). The aim of this study was to determine whether cytotoxic T lymphocytes (CTLs) recognize CDR3-derived peptides. METHODS: CTL (CD8 +) cell lines that could lyse two CTCL patients’ own tumor cells were first grown and then tested for their ability to respond to synthetic peptides derived from the TCRCDR3 sequence of the autologous malignant cells presented by the original B lymphocytes . Results: CTL secreted tumor necrosis factor (TNF @), which responded to its own TCR beta chain-specific peptide but did not respond to peptides or control peptides derived from the idiotypes of other TCR beta chains. Monoclonal antibodies against MHC class I molecules (W6 / 32) blocked their peptide recognition. CONCLUSIONS: CTLs first identified and responded to specific MHC class I-related peptides from malignant lymphocyte clones with CTCL-specific individual clones, and suggested that the stimulatory peptides originate from the TCRβ chain-idiotypic region. This study establishes this mechanism by which other T cells can mediate a given antigen-specific T cell. The identification of tumor-specific epitopes on CTCL may help to develop potentiating or initiating CD8-mediated?