Contribution of CD4(+ )and CD8(+) T-cells in contact hypersensitivity and allergic contact dermatitis.

Contribution of CD4(+ )and CD8(+) T-cells in contact hypersensitivity and allergic contact dermatitis.
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DOI:
10.1586/1744666x.1.1.75
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发表时间:
2005-05-01
影响因子:
4.4
通讯作者:
Nicolas, Jean-Francois
Nicolas, Jean-Francois
中科院分区:
医学3区
文献类型:
--
作者:
Vocanson, Marc;Hennino, Ana;Nicolas, Jean-Francois

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变态反应性接触性皮炎,又称接触性超敏,是最常见的炎症性皮肤病之一,以红肿、丘疹、水泡为特征,其次为鳞屑和干燥。过敏性接触性皮炎是在皮肤接触非蛋白化学物质半抗原时引起的,由半抗原特异性T细胞介导的皮肤迟发性超敏反应。在致敏阶段,CD4(+)和CD8(+)T细胞前体通过皮肤树突状细胞呈递半抗原肽在引流的淋巴结中被激活。随后在遥远的皮肤部位进行半抗原涂抹,可在挑战部位诱导特定T细胞的招募和激活。这会导致角质形成细胞的凋亡、炎症细胞的募集和临床症状的发展。近10年来的实验研究表明,在正常接触性超敏反应中,CD8(+)1型T细胞通过细胞毒作用和干扰素-γ的产生成为接触性超敏反应的效应细胞,而CD4(+)T细胞则被赋予下调调节功能。后者可能对应于最近描述的CD4(+)CD25(+)调节性T细胞群。然而,在某些情况下,特别是当存在CD8(+)T细胞池缺陷时,CD4(+)T细胞可以是接触性超敏反应的效应细胞。正在进行的研究将不得不证实,人类变态反应性接触性皮炎的病理生理学与小鼠接触性超敏反应相似,而对常见弱半抗原的接触超敏反应与报道的强半抗原相似。
Allergic contact dermatitis, also referred to as contact hypersensitivity, is one the most frequent inflammatory skin diseases, and is characterized by redness, papule and vesicles, followed by scaling and dryness. Allergic contact dermatitis is elicited upon skin contact with nonprotein chemicals, haptens, and corresponds to a cutaneous delayed type hypersensitivity reaction, mediated by hapten-specific T-cells. During the sensitization phase, both CD4(+) and CD8(+) T-cell precursors are activated in the draining lymph nodes by presentation of haptenated peptides by skin dendritic cells. Subsequent hapten painting on a remote skin site induces the recruitment and activation of specific T-cells at the site of challenge. This leads to apoptosis of keratinocytes, recruitment of inflammatory cells and development of clinical symptoms. Experimental studies from the last 10 years have demonstrated that, in normal contact hypersensitivity responses to strong haptens, CD8(+) type 1 T-cells are effector cells of contact hypersensitivity through cytotoxicity and interferon-gamma production, while CD4(+) T-cells are endowed with downregulatory functions. The latter may correspond to the recently described CD4(+)CD25(+) regulatory T-cell population. However, in some instances, especially when there is a deficient CD8(+) T-cell pool, CD4(+) T-cells can be effector cells of contact hypersensitivity. Ongoing studies will have to confirm that the pathophysiology of human allergic contact dermatitis is similar to the mouse contact hypersensitivity and that the contact hypersensitivity response to common weak haptens, most frequently involved in human allergic contact dermatitis, is similar to that reported for strong haptens.