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Absence of expression of class II major histocompatibility complex determinants on keratinocytes in bullous pemphigoid
Author(s) -
VENNING V.A.,
DHAN D.,
WOJNAROWSKA F.
Publication year - 1992
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1111/j.1365-2133.1992.tb15117.x
Subject(s) - bullous pemphigoid , pemphigoid , keratinocyte , immunology , medicine , major histocompatibility complex , dermatology , histocompatibility , biology , antigen , antibody , genetics , human leukocyte antigen , cell culture
Summary Aberrant expression of class 11 products of the major histocompatibility complex (HLA‐D locus antigens) occurs on keratinocytes in several inflammatory dermatoses and on thyroid epithelial cells in autoimmune thyroiditis. The functional significance of aberrant HLA‐D expression is unclear but it has been hypothesized that epithelial cells bearing these determinants may act as antigen‐presenting cells for autoantigens. The aim of the present study was to investigate the pathogenesis of bullous pemphigoid using immunohistotochemical methods to determine whether the HIA‐D locus antigens are aberrantly expressed on keratinocytes in lesional and uninvolved skin. A panel of monoclonal antibodies to each of the HLA‐D subregions (DR, DP and DQ) and to Langerhans cells was used. Epidermat expression of the HLA‐D locus antigens was similar in patients and controls, and there was no significant increase in expression in lesional skin compared with uninvolved skin in six out of nine patients. In three out of nine patients slight enhancement of epidermal HLA‐D expression in lesional epidermis corresponded to increased Langerhans cells rather than expression on keratinocytes. HLAD locus antigens are absent from keratinocytes in bullous pemphigoid skin and aberrant expression of these determinants cannot therefore be implicated in antigen presentation.