Cutaneous leukocytoclastic vasculitis: the role of lymphocytes and related immune markers.

Abstract

IntroductionApart from neutrophils, other immune cells may play a significant pathogenetic role in cutaneous leukocytoclastic vasculitis (CLV).AimTo investigate lymphocytes and related immunological factors in patients with CLV requiring systemic glucocorticosteroid treatment.Material and methodsFourteen patients with severe idiopathic CLV were treated with systemic prednisolone in a tapered dose regimen. Ten healthy individuals served as controls. At baseline and post-treatment, we studied inducer/helper and suppressor/cytotoxic T lymphocytes, B lymphocytes, natural killer cells, CD4+CD25++CD127– cells, CD4+CD25+CD39+ cells and FOXP3, transforming growth factor β1 (TGF-β1) and interleukin-10 (IL-10) mRNA levels in the blood using flow cytometry and real time polymerase chain reaction (RT-PCR), respectively. On immunohistochemistry, we studied CD4, CD8, granzyme B, TGF-β1, and IL-10.ResultsFlow cytometry did not show significant differences. The RT-PCR revealed that TGF-β1 mRNA expression was significantly higher after therapy when compared to baseline and controls. On immunohistology, baseline CLV lesions showed significantly more CD4+ lymphocytes than post-treated CLV and controls. CD8+ expression was significantly higher after therapy when compared to baseline and controls. Baseline granzyme B was significantly increased when compared to treated CLV and controls. The IL-10 expression of treated CLV was significantly increased when compared to baseline CLV and; baseline CLV IL-10 expression was significantly increased as compared to controls.ConclusionsCirculating T regulatory cells do not play a significant role in the pathogenesis of CLV. T helper cells and granzyme B seem to be involved in the inflammatory cutaneous process of CLV. A resolution of CLV observed after glucocorticosteroid treatment may be mediated via up-regulation of TGF-β1 and IL-10 in different compartments.