CD23 AND IGE EXPRESSION DURING THE HUMAN IMMUNE-RESPONSE TO CUTANEOUS LEISHMANIASIS - POSSIBLE ROLE IN MONOCYTE ACTIVATION

Leishmania brasiliensis causes cutaneous leishmaniasis (CL) in humans. During this infection, a variety of inflammatory mediators are produced by T cells and monocytes/macrophages. In the present study, we analysed serum IgE levels and their correlation with in situ expression of the low affinity receptor for IgE (FcepsilonRII/CD23) in patients infected with L. brasiliensis before and following therapy. These analyses were compared to in situ expression of tumour necrosis factor-alpha (TNFalpha), interleukin 3 (IL3), interferon-gamma (IFNgamma) and IL4. Disease-free individuals from the same endemic area sensitized with L. brasiliensis antigens were also included in this work. Our data indicate that during infection, serum levels of IgE and TNFalpha increased and correlated with elevated in situ expression of CD23, IL4 and TNFalpha mRNA. This expression disappeared following successful treatment, but persisted in patients resistant to anti-leishmania therapy. Patients resistant to therapy differed from other cases by a dramatic decrease in their in vivo expression of IFNgamma protein. Analysis of CD23 function in purified human monocytes indicated that this antigen mediates IgE/anti-IgE-dependent TNFalpha production. These data suggest a possible in vivo role of CD23 in acute immune responses in human CL.