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T‐cell receptor Vβ usage by lesional lymphocytes in oral lichen planus
Author(s) -
Thomas D. W.,
Stephens P.,
Stephens M.,
Patten D. W.,
Lim S. H.
Publication year - 1997
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1111/j.1600-0714.1997.tb00031.x
Subject(s) - oral lichen planus , t cell receptor , superantigen , beta (programming language) , t lymphocyte , population , immunology , microbiology and biotechnology , t cell , antigen , biology , pathology , medicine , immune system , environmental health , computer science , programming language
To determine whether the T‐cell inflammatory infiltrate in oral lichen planus (OLP) represents a selective activation and expansion of a limited repertoire of T‐cell receptor (TCR) specific T‐cells. Vβ gene expression was investigated in lesional T‐lymphocytes in OLP. A reverse transcriptase‐polymerase chain reaction (RT‐PCR) technique was used to amplify the 24 major Vβ gene sub‐families of infiltrating mucosal lymphocytes and peripheral blood mononuclear cells (PMNC) in seven patients with reticular OLP and four healthy control patients. Specificity of amplified products was confirmed by Southern blotting with a Cp internal probe. TCR Vβ usage by lesional T‐cells in OLP was markedly heterogeneous 5–23 Vβ sub‐families). In 6/8 patients with OLP. Vβ usage was restricted with 20/25 sub‐families detected: only one of the Vβ sub‐families (Vβ 8) was present in all of the OLP patients demonstrating TCR Vβ restriction. In contrast. TCR Vβ usage was unrestricted in PMNC from OLP patients and controls (23/25 sub‐families detected). In three patients, certain Vβ sub‐families (Vβ13, Vβ14 & Vβ15) were present in the lesional T‐cell population but were under‐represented in PMNC. These results suggest a selective Vβ gene usage by lesional infiltrating T‐cells in oral lichen planus. The non‐uniformity of Vβ restriction in lesional T‐cells does not support the concept of a common superantigen in OLP and reflects the heterogeneity of the disease.