The immunological basis of lichenoid tissue reaction
The immunological basis of lichenoid tissue reaction
复制标题
DOI：
10.1016/j.autrev.2004.11.005
复制
发表时间：
2005-04-01
影响因子：
13.6
通讯作者：
Mizukawa, Y
中科院分区：
文献类型：
--
作者：
Shiohara, T;Mizukawa, Y
T细胞对表皮的自身免疫攻击是苔藓样组织反应（LTR）的主要病理事件。LTR中表皮损伤的严重程度取决于T细胞活化的强度和持久性与表皮细胞保护免受攻击的能力之间的相对平衡。在自然疾病过程中，由一些外源性试剂激活的T细胞从血液迁移到皮肤部位并侵入表皮。虽然这种导致表皮破坏的T细胞向表皮迁移是一个复杂的多步骤过程，但在固定性药疹（FIDE）中可以绕过。因此，FDE是研究LTR发病机制的最简化的疾病模型，因为大量效应CD 8（+）T细胞作为稳定群体持续存在于静息病变中而不引起表皮损伤，并且这些T细胞的激活导致局部表皮损伤只能在给予致病药物后诱导。基于对这些CD 8（+）皮肤驻留T细胞观察到的发现，我们假设在病毒感染期间引发的CD 8（+）T细胞可以进化成长寿的效应记忆表型T细胞;它们随后将特异性或非特异性地被捕获在发炎的皮肤部位，并最终作为稳定的群体持续存在。然而，一旦与外源性刺激（如药物或自身抗原）发生交叉反应，它们就会成为表皮损伤的效应物，如各种苔藓样皮肤病。(c)2004 Elsevier B. V.保留所有权利。
An autoimmune attack by T cells on the epidermis is the primary pathological event in the lichenoid tissue reaction (LTR). The severity of epidermal damage in the LTR is dependent on the relative balance between the intensity and perpetuation of T cell activation and the capacity of epidermal cells to protect from the attack. In natural disease processes, T cells activated by some exogenous agents migrate from the blood to the skin sites and invade the epidermis. Although this epidermotropic migration of T cells resulting in epidermal destruction is a complicated multistep process, this can be bypassed in fixed drug eruption (FIDE). Thus, FDE is the most simplified disease model for investigating the pathogenesis of the LTR, in that large numbers of effector CD8(+) T cells persist as a stable population in the resting lesions without causing epidermal damage and activation of these T cells resulting in localized epidermal injury can only be induced after administration of the causative drugs. Based on the findings observed with these CD8(+) skin-resident T cells, we hypothesize that CD8(+) T cells primed during viral infections could evolve into long-lived effector memory phenotype T cells; they would be subsequently trapped either specifically or nonspecifically in the inflamed skin sites and eventually persist as a stable population. Once cross-reacted with exogenous stimuli, such as drug or self-antigens, however, they would become effectors of epidermal damage as seen in various lichenoid skin diseases. (c) 2004 Elsevier B.V. All rights reserved.