케모카인과 염증성 피부질환

Abstract

Chemokines are believed to be involved in the specific recruitment of immune cells into the lesions of inflammatory skin diseases such as allergic contact dermatitis (ACD), psoriasis and atopic dermatitis (AD) in which a T cell mediated mechanism plays a significant role in the pathogenesis. Recent advances in chemokine transgenic and knock-out mice can be used to elucidate the role that chemokines play in contact hypersensitivity (CHS). Psoriasis and AD animal models can also help to understand the pathogenic mechanism. However, extrapolating this information from animal models falls short of a full understanding of the immunopathogenesis of these diseases. Human ACD is usually studied in the aspect of the efferent (elicitation) phase, but CHS animal models traditionally focus on the afferent (sensitization) phase. On the other hand, psoriasis and AD animal models cannot imitate the disease completely. Therefore, a precise comparative analysis of the patients´ skin samples from these inflammatory skin diseases is necessary to understand the fundamental differences in these diseases. In ACD lesions IL-8, MCP-1, IP-10, Mig and I-TAC are believed to be involved in the pathogenic process. However, I-309 is considered to be a chemokine involved in the suppressive phase of ACD by recruiting regulatory T cells. In Psoriasis, IL-8, IP-10, Mig and MIP-3α appear to play a significant role in the pathogenic process. However, eotaxin, RANTES, MCP-4, TARC and MDC seem to be significant participants in the pathogenesis of AD. This review focuses on the general concept of chemokines, and the differences in chemokine expression in the lesions from inflammatory skin diseases.