Abstract
HIV coinfection modifies the clinical course of leishmaniasis by promoting a Th2 pattern of cytokine production. However, little information is available regarding the lymphocytic response in untreated coinfected patients. This work presents the immunophenotyping of Leishmania-stimulated T cells from a treatment-naÏve HIV+ patient with ML. Leishmania braziliensis antigens induced CD69 expression on CD3+CD4+ and CD3+CD8+ cells. It also increased IL-4 intracellular staining on CD3+CD4+GATA3- population and decreased the percentage of CD3+CD4+IL-17+ cells. This suggests that modulations in the IL-4R/STAT6 pathway and the Th17 population may serve as parasitic evasion mechanisms in HIV/ML. Further studies are required to confirm these results.
Highlights
Human protection against localized cutaneous leishmaniasis (LCL) due to Leishmania (Viannia) braziliensis (Lb) is dependent on an efficient T helper lymphocyte 1 (Th1) response, whereas susceptibility is associated with an increased Th2 and T regulatory (Treg) profile[1,2]
In a late stage AIDS-associated Mucosal leishmaniasis (ML) patient, the low lymphocyte proliferative response and IFN-γ production were restored after the first specific immunochemotherapy course
This restoration was dependent on predominating CD8+ rather than CD4+ responding T cells[6]. Another HIV+/ML case series showed that circulating CD4+ T cell count was < 150 cells/mm[3] and that the leishmaniasis clinical outcome showed strong variability among the patients[5]
Summary
Human protection against localized cutaneous leishmaniasis (LCL) due to Leishmania (Viannia) braziliensis (Lb) is dependent on an efficient T helper lymphocyte 1 (Th1) response, whereas susceptibility is associated with an increased Th2 and T regulatory (Treg) profile[1,2].
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