engleski

TOLL-LIKE RECEPTORS AND REGULATORY T CELLS IN SYSTEMIC LUPUS ERYTHEMATOSUS

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by the presence of autoantibodies to different nucleus components. The generation and survival of autoreactive B cells could result from the loss of immune tolerance, molecular mimicry, and inappropriate clearance of apoptotic cells or changes in regulatory T cell (Treg) function. Infections have been known to trigger and/or aggravate SLE. Invading microorganisms are recognized by the innate immune system via Toll-like receptors (TLRs). TLR activation also modulates the function of Tregs. We investigated the expression of TLRs and percentage of Tregs in peripheral blood of SLE patients and controls by flow cytometry using three or four-color immunofluorescence staining. Patients were analyzed at 3 time-points: before therapy, 3 weeks after the onset of corticosteroid therapy, and again after 3 months, when chloroquine was introduced into the protocol. Also, we performed a two-year follow-up to examine the effect of therapy on the frequency of Foxp3+ Tregs in a newly diagnosed SLE patient. TLR2 expression on monocytes decreased after 3 weeks and 3 months of therapy in comparison to healthy controls. TLR9 expression on B cells increased after 3 weeks of therapy. The percentage of Foxp3+ Tregs increased after 3 weeks of therapy but decreased again at two years. This was accompanied by slight deterioration of the patient’ s symptoms. Further experiments are under way to establish the importance of TLR and Treg as markers of disease activity and to investigate the possible immunomodulatory effects of drugs used in treatment of SLE.

Toll-like receptors; B cells; regulatory T cells; Foxp3

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