Lichen Planus Annularis: An Immunohistochemical Study

Abstract

Lichen planus annularis is a relatively rare skin manifestation of lichen planus. The mechanisms in the formation of annular lesions are not fully understood. We reported here a 57-year-old female with this disease. The eruption initially occurred as lichen-papules, then enlarged (bean-sized, umbilicated small plaques), and finally developed annular manifestations. We performed immunohistochemical examinations of specimens taken from different types of eruptions. In all specimens, HLA-DR was expressed in the focal keratinocytes adjacent to the dermal HLA-DR positive cell infiltration. Both in the initial papule and in the final annular lesion, expression of ICAM-1 was present only in the keratinocytes above the dermal cell infiltration, similar to HLA-DR. It is of interest that, in the umbilicated small plaques, the peripheral epidermis other than the central site extensively reacted to ICAM-1. LFA-1 expression was most prominent in the mononuclear cells impinging on the dermo-epidermal junction in all specimens. In addition, in the periphery of the umbilicated small plaques, which showed no bandlike dense cell infiltration nor degeneration of basement membrane, TNF-alpha, but not LFA-1, was positive in the infiltrated cells of the upper dermis. These results suggest that expressions of ICAM-1 and TNF-alpha in the peripheral keratinocytes and dermal infiltrated cells are important molecular events in the mechanisms of formation of the annular lesions.

Lichen Planus and Sjögren‐type Sicca Syndrome in a Patient with Chronic Hepatitis C

“…In the focal cellular infiltrate in the salivary glands, which is the specific feature of Sjogren-type sicca syndrome, CD45RO+ cells were also prominent in most of the foci, and HLA-DR an tigens were expressed mainly in those foci. These results seem to agree with those of previous immunopathologic studies of LP (15,22) and Sjogren's syndrome (14,23), suggesting that the cellular infiltration of LP and Sjogren-type sicca syndrome in this case may be attributable to a common pathogenetic mechanism. This suggestion may be supported by the clinical data showing that the normalization of high serum amylase level, in which salivary amylase predominated, paralleled the improvement in the oral LP.…”

Annular Atrophic Lichen planus

“…Although the mechanism in the formation of annular lesions in lichen planus is not fully understood, recent immunohistochemi cal studies have suggested that intercellular adhesion mole cule 1 expression in the peripheral kératinocytes of active lesions of annular lichen planus may be an important initia tor in the adhesion of lymphocytes to the epidermis. These results seem to indicate that peripheral expression of inter cellular adhesion molecule 1 can be involved as a crucial early molecular event in the process of annular formation [5]. Another unusual variant of lichen planus is atrophic lichen planus, which occurs after the resolution of long time lesions of lichen planus [6, 7| and is interpreted as a result of thinning of the epidermis and fibrosis of the papil Received: May 28, 1993 Accepted: October 7, 1993 lary dermis [8].…”

Leprosy: accessory immune system as effector of infectious, metabolic, and immunologic reactions

“…The proliferation potential is greatly reduced and bacterial processing proceeds up to antigenic peptide levels. Cell‐mediated immune responses with memory CD4+ Th‐1 and CD8+ T‐lymphocyte expression may result and lead to epithelioid cell granuloma formation 14–16 or a lichenoid reaction 60–67 . CD4+ Th‐1 lymphocyte stimulation induces interferon‐γ (IFN‐γ) and interleukin‐2 (IL‐2) release, which promotes and accelerates phagolysosome processing within newly infected macrophages.…”