Abstract
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 (Fc epsilon RII/CD23) in patients infected with L. brasiliensis before and following therapy. These analyses were compared to in situ expression of tumour necrosis factor-alpha (TNF alpha), interleukin 3 (IL3), interferon-gamma (IFN gamma) 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 TNF alpha increased and correlated with elevated in situ expression of CD23, IL4 and TNF alpha 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 IFN gamma protein. Analysis of CD23 function in purified human monocytes indicated that this antigen mediates IgE/anti-IgE-dependent TNF alpha production. These data suggest a possible in vivo role of CD23 in acute immune responses in human CL.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
