Abnormal Expression Of Cell Differentiation Markers In Lichen Planus Lesions

Abstract Transglutaminase of keratinocyte(TGK), Filaggrin, Keratin17 and Keratin16 are important markers of hyperproliferation and differentiation of keratinocytes. Under pathological conditions especially in psoriasis and wound healing, abnormal expression of these makers can be caused by maladjusted growth and differentiation of keratinocytes. The pathological changes of lichen planus are similar to those of psoriasis. This means that abnormal hyperproliferation of keratinocytes and infiltration of inflammatory cells present in both cases. In this study, the in situ expression of TGk, Filaggrin, K17 and K16 in lichen planus was dectected with immunohistochemistry and then compared with that in the lesional psoriatic epidermis.TGK was positively stained only in stratum granulosum of normal epidermis . However, the positively stained area extended to prickle cell layer in defected skin of lichen planus and the staining intensity was markedly stronger than that in normal skin. The distribution of TGK in psoriasis was analogous to lichen planus. The expression of Filaggrin was limited to stratum corneum in normal epidermis. In defected skin of Lichen planus besides above area, Filaggrin was also expressed at upper part of prickle cell layer and the color intensity was higher. In contrast, only at wedge of incrassate stratum granulosum there was marked positively area in defected skin of psoriasis. In normal epidermis Keratin 17 was stained negatively and Keratin 16 was faintly positive at the basal cell layer. While in Lichen planus and psoriasis, Keratin 17 and Keratin 16 mainly distributed at the prickle cell layer , which is much different from that in normal skin control. These findings suggest that there are obviously abnormal hyperproliferation and differentiation of keratinocytes in defected skin of lichen planus. The advanced expression of Filaggrin may start the mechanism of apoptosis ahead of time and the premature expression of TGK may accelerate the formation of cornified cell membrane, which will speed up the terminal differentiation of keratinocytes. Consequently, the hyperproliferative keratinocytes differentiate and exfoliate. This increased apoptosis of cells is beneficial to eliminate the excessive hyperproliferative kerationcytes.The expression of Keratin17 and Keratin16 in lesional skin of lichen planus may be not only hyperproliferation markers of keratinocytes ,but also the result of up-regulation by cytokines from infiltrated inflammatory cells.At the areas of normal skin proxmate lesional skin in lichen planus ,although there are no pathological changes under microscrope,the terminal differentiation of keratinocytes may have been abnormal.