Allergic contact dermatitis is a primarily T-cell-mediated inflammatory skin disease induced by exposure to small molecular-weight haptens, which covalently bind to proteins. The abundance of cutaneous T cells that recognize CD1a antigen-presenting molecules raises the possibility that MHC-independent antigen presentation may be relevant in some hapten-driven immune responses. Here we examine the ability of contact sensitizers to influence CD1-restricted immunity. Exposure of human antigen-presenting cells such as monocyte-derived dendritic cells and THP-1 cells to the prototypical contact sensitizer dinitrochlorobenzene potentiated the response of CD1a- and CD1d-autoreactive T cells, which released a vast array of cytokines in a CD1- and TCR-dependent manner. The potentiating effects of dinitrochlorobenzene depended upon newly synthesized CD1 molecules and the presence of endogenous stimulatory lipids. Further examination of a broad panel of contact sensitizers revealed 1,4-benzoquinone, resorcinol, isoeugenol, and cinnamaldehyde to activate the same type of CD1-restricted responses. These findings provide a basis for the antigen-specific activation of skin-associated CD1-restricted T cells by small molecules and may have implications for contact sensitizer-induced inflammatory skin diseases.

中文翻译：

---

接触敏化剂触发人CD1自反应性T细胞反应。

过敏性接触性皮炎是一种主要的T细胞介导的炎症性皮肤病，是由于暴露于小分子半抗原引起的，该小分子半价与蛋白质共价结合。识别CD1a抗原呈递分子的大量皮肤T细胞增加了MHC依赖性抗原呈递可能与某些半抗原驱动的免疫反应有关的可能性。在这里，我们研究了接触敏化剂影响CD1限制性免疫的能力。人类抗原呈递细胞（例如单核细胞衍生的树突状细胞和THP-1细胞）暴露于原型接触敏化剂二硝基氯苯可增强CD1a和CD1d自反应性T细胞的反应，从而释放CD1和CD1d中大量的细胞因子。 TCR依赖方式。二硝基氯苯的增效作用取决于新合成的CD1分子和内源性刺激性脂质的存在。进一步对一系列接触敏化剂进行了检查，结果发现1,4-苯醌，间苯二酚，异丁香酚和肉桂醛可以激活相同类型的CD1限制性反应。这些发现为小分子对皮肤相关的CD1限制性T细胞的抗原特异性活化提供了基础，并且可能对接触致敏剂引起的炎症性皮肤病有影响。