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

Leishmania brasiliensis causes cutaneous leishmaniasis (CL) in humans. During this infection, a variety of inflammatory mediators are produc ed by T cells and monocytes/macrophages. In the present study, we anal ysed serum IgE levels and their correlation with in situ expression of the low affinity receptor for IgE (FcepsilonRII/CD23) in patients inf ected with L. brasiliensis before and following therapy. These analyse s 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 indic ate that during infection, serum levels of IgE and TNFalpha increased and correlated with elevated in situ expression of CD23, IL4 and TNFal pha mRNA. This expression disappeared following successful treatment, but persisted in patients resistant to anti-leishmania therapy. Patien ts resistant to therapy differed from other cases by a dramatic decrea se in their in vivo expression of IFNgamma protein. Analysis of CD23 f unction in purified human monocytes indicated that this antigen mediat es IgE/anti-IgE-dependent TNFalpha production. These data suggest a po ssible in vivo role of CD23 in acute immune responses in human CL.