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The effect of methotrexate on the expression of cell adhesion molecules and activation molecule CD69 in psoriasis
Author(s) -
TorresÁlvarez B,
CastanedoCazares JP,
FuentesAhumada C,
Moncada B
Publication year - 2007
Publication title -
journal of the european academy of dermatology and venereology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.655
H-Index - 107
eISSN - 1468-3083
pISSN - 0926-9959
DOI - 10.1111/j.1468-3083.2006.01916.x
Subject(s) - psoriasis , cell adhesion molecule , cd8 , medicine , cell adhesion , cytotoxic t cell , intercellular adhesion molecule 1 , immunology , t cell , soluble cell adhesion molecules , methotrexate , cell , immune system , cancer research , chemistry , in vitro , biochemistry
Background The mechanism of the action of methotrexate (MTX) in the treatment of psoriasis has not been completely elucidated. Objective To assess the effect of MTX on the expression of intercellular adhesion molecule‐1 (ICAM‐1), vascular cell adhesion molecule‐1 (VCAM‐1), E‐selectin, activation molecule CD69 and T‐cell phenotype in skin specimens from patients with psoriasis. Methods We performed an immunohistochemical analysis of the expression of T‐cell phenotype and cell adhesion/activation molecules in skin biopsies from patients with psoriasis treated with a fixed dose of MTX (12.5 mg/week). To determine data on the epidermal/dermal T‐cell infiltration we carried out a manual quantification. Results Skin samples prior to therapy showed a moderate to severe inflammatory infiltrate, mainly due to T lymphocytes with a helper/inducer (CD4) phenotype. Most of these cells also expressed ICAM‐1 and VCAM‐1. Blood vessels showed expression of E‐selectin and VCAM‐1, and keratinocytes were positive for ICAM‐1 staining. The cell infiltrate was reduced after therapy, as well as the expression of cell adhesion molecules. However, we also noted the persistence of the T lymphocyte phenotype CD8 + , expressing the CD69 activation molecule, after the MTX treatment. Conclusions MTX downregulates the expression of some adhesion molecules, a phenomenon that may contribute to its anti‐inflammatory therapeutic effect in psoriasis. The infiltrating T cells post‐treatment have an activated cytotoxic phenotype, which may suggest a pathogenic role in the continuation and/or recurrence of psoriasis.