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O. Kose, J. Stewart, A. Waseem, A. Lalli, F. Fortune, Expression of cytokeratins, adhesion and activation molecules in oral ulcers of Behçet's disease, Clinical and Experimental Dermatology, Volume 33, Issue 1, 1 January 2008, Pages 62–69, https://doi.org/10.1111/j.1365-2230.2007.02558.x
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Summary
Background. Behçet's disease (BD) is a multisystemic inflammatory disorder of which oral aphthous ulceration is a major feature.
Aims/hypothesis. This study sought to determine the role of cytokeratins, differentiation and proliferation markers, γδ T‐cell adhesion and activation molecules, and apoptotic markers in oral ulcers of this disease.
Methods. Expression patterns for cytokeratins (K1, K6, K14, K15, K16), integrins (β1 and α6), CD3 T‐cell and γδ T‐cell adhesion and activation markers [CD40, CD44, CD54, ICAM‐1, CD58, leucocyte function‐associated antigen (LFA)‐3, vascular cell adhesion molecule‐1 (VCAM‐1), CD86], and cellular proliferation and differentiation markers (Ki67 and involucrin), and apoptotic markers (CD95 and Bcl‐2) in oral ulcers of nine patients with BD and four healthy controls were analysed by immunohistochemistry.
Results. K14, K15 and involucrin expression were unchanged, whereas Ki67, the proliferation marker, was reduced by around 50%. K1, K6, K16, β1 integrin and the apoptotic marker CD95 were upregulated, whereas α6 integrin and Bcl‐2 were downregulated in BD samples. CD3 and γδ T‐cell expression and other adhesion molecules including CD44, CD86, CD58 (LFA‐3), VCAM‐1 and intercellular adhesion molecule‐1 (CD54) were upregulated, whereas CD40 showed little change.
Conclusions. Our data demonstrates changes in cell–cell and cell–extracellular matrix interactions that affect cell homeostasis and may participate in the formation of oral ulcers in BD.