RESUMO
Increased serum levels of IL-2 and sIL-2R can be demonstrated in patients with active MS, a finding that strongly supports the hypothesis of a systemic T cell activation in such patients. However, IL-2 may play a crucial role in MS immunopathology by activating endothelial cells, as suggested by the vascular leak syndrome complicating hrIL-2 therapy. Early BBB impairment and focal perivascular edema that characterize MS lesions may be the effect of an IL-2-induced cytokine cascade.
Assuntos
Endotélio Vascular/fisiologia , Interleucina-2/farmacologia , Esclerose Múltipla/metabolismo , Barreira Hematoencefálica , Citocinas/fisiologia , Endotélio Vascular/efeitos dos fármacos , Humanos , Interleucina-2/fisiologia , Esclerose Múltipla/sangue , Esclerose Múltipla/imunologiaRESUMO
Lymphocyte subpopulations, T cell activation antigens, and serum levels of interleukin 2 (IL-2) and soluble IL-2 receptor (sIL2R), were studied in relapsing-remitting MS (RR-MS) patients before and after high-dose steroid therapy. Prior to therapy, a minority of patients showed increased HLA-DR antigen expression, and an increased number of CD16+ and CD19+ cells. Steroid treatment induced a significant increase in HLA-DR and CD19 expression, a significant reduction in CD16+, CD57+, and CD8+ CD57+ cells, and a slight, non-significant, decrease in IL-2 and sIL-2R levels and CD25 expression on CD4+ T lymphocytes.