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Abstract
Lichen planus is a chronic inflammatory papulosquamous skin disease characterized by epidermal basal cell damage and a particular band-like infiltrate predominantly of T cells in the upper dermis. Although the pathogenesis is not yet clear, lichen planus is recognized as a T-cell-mediated disease. Both CD4 and CD8+ T cells are found within lichen planus lesions. It seems that CD4 cells predominantly infiltrating the dermis subsequently activate cytotoxic CD8 cells that cause epidermal cell damage. T cell lines from lesional skin in LP contain specific type of T- lymphocytes (gamma delta (γ δ) T cells) which are not found in normal skin. This subtype of lymphocytes is known to respond to specific antigenic portion of certain heat shock protein (HSP) molecules >Heat shock proteins (HSPs) are expressed by most living cells and play fundamental roles in many biological processes. Although they are induced by any form of stress, it is known that HSPs are constitutively expressed in normal unstressed) cells playing a fundamental role in many biological processes such as control of apoptosis, protection against ultraviolet (UV) damage, wound healing/repair, regulation of steroid aporeceptors, kinases, and other protein remodelling processes The aim of this work was to investigate the expression of HSP60 in lesions of LP and comparing it with normal skin, to explain its role in LP pathogenesis Forty LP patients and 10 control subjects of apparently normal skin were selected. All patients were subjected to detailed history taking, and dermatological examination. The patients’ ages ranged from 10-69 years, with amean ± SD of 33.68 years ± 15.07. They were 21 males (52.5%), and 19 females (47.5%) with a male: female ratio = 1.1: 1. There were no statistically significant difference between LP cases and controls as regards age and sex.