Expression of the CD54 (ICAM‐1) and CD11 a (LFA‐1) adhesion molecules in oral mucosal inflammation

Abstract

Previous studies of chronic dermatoses have suggested that expression of the CD54 cell surface antigen (intercellular adhesion molecule-1, ICAM-1) by keratinocytes is a feature of chronic inflammation. However, whether such expression is a prerequisite for intraepithelial migration of lymphocytes is unclear. The present study evaluated the expression of CD54 and its ligand, CD11a (lymphocyte function-associated antigen, LFA-1) in oral lesions of lichen planus, recurrent aphthous stomatitis, secondary Sjögren's syndrome and traumatic ulceration using an immunoperoxide technique. In 33 of 56 lesions examined, substantial numbers of CD11a + cells were present within oral mucosal epithelium despite an absence of detectable keratinocyte CD54 antigen expression. Consequently, CD54/CD11a adhesion interactions may not be critical in the initiation of oral mucosal inflammation.

Extravasation of leukocytes assessed by intravital microscopy: Effect of thalidomide

“…In order to explain the focal nature of aphthous lesions, however, the role of adhesion molecules in clinical vasculitis needs further study. So far, only an increased expression of ICAM-1 and its counter-ligand, LFA-1, has been shown by immunohistochemical methods in biopsies obtained from recurrent aphthous stomatitis lesions [21].…”

Recurrent Aphthous Stomatitis

“…The aggregation of lymphocytes is probably mediated by the adhesion molecules-intercellular adhesion molecule 1 (ICAM-1) and lymphocyte function-antigen-3 (LFA-3)-binding to their counterpart ligands LFA-1 and CD-2 on lymphocytes (Hayrinen-Immonen et al, 1992;Verdickt et al, 1992). ICAM-1 is expressed on the submucosal capillaries and venules, suggesting that it may control the trafficking of leukocytes into the submucosa (Savage et al, 1986;Eversole, 1994), while LFA-3 and its counterpart ligand CD-2 are likely to be involved in T-cell activation in RAS.…”

Update On Oral Lichen Planus: Etiopathogenesis and Management

“…ICAM-l is present on the endothelium of blood vessels of normal and LP-involved oral mucosa (Walton et al, 1994), but there is often increased expression on basal and parabasal keratinocytes, intra-epithelial Langerhans cells, macrophages, and CD4+ and CD8+ lymphocytes within the lamina propria in LP (Simon and Hunyadi, 1990;Eversole et al, 1994;Walton et al, 1994). While increased keratinocyte ICAM-1 expression is not always present (Walsh et al, 1990a;Verdickt et al, 1992), elevation of ICAM-1 expression on keratinocytes may correlate with sites of T-cell infiltration into the epithelium (Griffiths et al, 1989a;Konter et al, 1991;Boehncke et al, 1992) and be induced by IFN-y or TNF.…”