Sosroseno W
Department of Dental Public Health, Faculty of Dentistry, Gadjah Mada University, Yogyakarta, Indonesia.
Asian Pac J Allergy Immunol. 1995 Dec;13(2):173-81.
Attempts have been made to elucidate the immunopathogenesis of contact allergy; yet, the exact mechanism by which nickel-induced allergic contact dermatitis (NACD) occurs is far from clear and is discussed herein. It seems to suggest that a direct nickel-MHC class II molecule binding on the skin antigen presenting cells such as Langerhans cells (LCs) would result in Th1 cell activation. Substances such as serotonin and cytokines such as TNF-alpha produced by activated mast cells may increase adhesion molecule expression and thus, enhance T cell trafficking in the skin. Cytokines such as IFN-gamma and IL-1 and perhaps IL-12 certainly play a crucial role in the activation of Th1 cells. Along with possible function of CD8 cells, downregulation of NACD may be mediated by suppressed function of LCs via the action of activated keratinocytes-derived IL-10. Inhibition of NACD can also be generated by feeding with nickel, suggesting that the induction of oral tolerance to nickel may be beneficial for an alternative immunotherapy of nickel allergy. Nevertheless, this testable model provides a direction for further investigation.
人们已尝试阐明接触性过敏的免疫发病机制；然而，镍诱导的过敏性接触性皮炎（NACD）发生的确切机制仍远未明确，本文将对此进行讨论。似乎有迹象表明，镍与皮肤抗原呈递细胞（如朗格汉斯细胞，LCs）上的II类主要组织相容性复合体（MHC）分子直接结合会导致Th1细胞活化。活化的肥大细胞产生的5-羟色胺等物质以及肿瘤坏死因子-α等细胞因子可能会增加黏附分子的表达，从而增强T细胞在皮肤中的运输。干扰素-γ、白细胞介素-1以及可能还有白细胞介素-12等细胞因子在Th1细胞的活化中肯定起着关键作用。除了CD8细胞可能发挥的作用外，NACD的下调可能是通过活化的角质形成细胞衍生的白细胞介素-10的作用，抑制LCs的功能来介导的。通过喂食镍也可以抑制NACD，这表明诱导对镍的口服耐受可能有利于镍过敏的替代免疫疗法。然而，这个可验证的模型为进一步研究提供了一个方向。
