Direct and indirect control of T-cell activation by keratinocytes.
Direct and indirect control of T-cell activation by keratinocytes.
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角质形成细胞直接和间接控制 T 细胞活化。
DOI：
10.1111/1523-1747.ep12315202
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发表时间：
1995
期刊：
影响因子：
--
通讯作者：
Nestle,FO
中科院分区：
文献类型：
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作者：
Nickoloff,BJ;Turka,LA;Mitra,RS;Nestle,FO
角质形成细胞可以作为抗原呈递细胞/辅助细胞发挥作用，并根据刺激的性质以三种不同的结果调节T细胞。在同种异体抗原的存在下，似乎在T细胞和角质形成细胞之间发生“无效”事件，既没有活化也没有诱导耐受。使用标称抗原，角质形成细胞诱导抗原特异性耐受。与此相反，与细菌衍生的超抗原，植物血凝素，或固定的CD 3单克隆抗体，角质形成细胞可以显着激活静息自体T细胞增殖和细胞因子释放。为了理解这些高度不同的反应，我们专注于T细胞活化的双信号模型，特别强调角质形成细胞表达的共刺激分子。这些第二信号，如B7和CD 28受体家族所强调的，为涉及角质形成细胞和T细胞的复杂相互作用提供了有用的见解。在这篇综述中，我们总结了最近的证据表明，角质形成细胞调节T细胞活化的直接和间接的方式，其相互表达和反应，涉及粘附分子，细胞因子，共刺激信号。随着免疫学和角质形成细胞生物学领域的研究势头持续增长，很可能CD 28：B7相互作用的操纵不仅将提供进一步理解皮肤免疫反应的复杂性的有用模型，而且还将作为涉及与角质形成细胞的异常反应的许多T细胞介导的疾病的新治疗机会的基础。
Keratinocytes can function as antigen-presenting cells/accessory cells and regulate T cells with three distinct outcomes, depending on the nature of the stimulus. In the presence of alloantigen, it appears that a "null" event takes place between T cells and keratinocytes, with neither activation nor induction of tolerance. Using nominal antigen, keratinocytes induce antigen-specific tolerance. In contrast, with bacterial-derived superantigens, phytohemagglutinin, or immobilized CD3 monoclonal antibody, keratinocytes can significantly activate resting autolo-gous T-cell proliferation and cytokine release. To understand these highly divergent responses, we focused on the two-signal model of T-cell activation, with particular emphasis on costimulatory molecules expressed by keratinocytes. Such second signals, as highlighted by the B7 and CD28 receptor families, provide useful insights into the complex interactions involving keratinocytes and T cells. In this review, we summarize recent evidence indicating that keratinocytes regulate T-cell activation in a direct and indirect manner by their mutual expression and responsiveness involving adhesion molecules, cytokines, and costimulatory signals. As investigative momentum continues to grow in the fields of immunology and keratinocyte biology, it is likely that manipulation of CD28:B7 interactions will not only provide a useful model to understand further the complexities of skin immune reactions, but will also serve as the basis for new therapeutic opportunities for numerous T-cell—mediated diseases that involve aberrant reactions with keratinocytes.J Invest Dermatol 105-.25S-29S, 1995