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The role played by dendritic cells (DCs) in Leishmania donovani infection is poorly understood. Here, we report that L. donovani amastigotes efficiently infect human peripheral-blood monocyte-derived DCs. Opsonization with normal human serum enhanced the infectivity of amastigotes and promastigotes only marginally. Surface attachment versus internalization was distinguished by incubation of DCs with live, fluorescein isothiocyanate-labeled parasites, followed by quenching with crystal violet. Infection with amastigotes was accompanied by DC maturation, as was evident from the up-regulation of maturation-associated cell-surface markers, the nuclear translocation of RelB, and the release of cytokines. Amastigote-primed DCs produced inflammatory cytokines in response to subsequent treatment with interferon- gamma or anti-CD40 monoclonal antibody. When cocultured, amastigote-infected DCs induced T helper cell type 1 (Th1) responses both in naive allogeneic CD4(+) T cells and in autologous CD4(+) T cells from patients with kala-azar and up-regulated the expression of T-bet. Our data reveal that infection with L. donovani amastigotes induces a Th1 cytokine milieu in both DCs and T cells.

the journal of infectious diseases (online. university of chicago press)/the journal of infectious diseases

<i>Leishmania donovani</i>Infection of Human Myeloid Dendritic Cells Leads to a Th1 Response in CD4<sup>+</sup>T Cells from Healthy Donors and Patients with Kala‐Azar

Leishmania donovaniInfection of Human Myeloid Dendritic Cells Leads to a Th1 Response in CD4+T Cells from Healthy Donors and Patients with Kala‐Azar

Leishmania donovaniInfection of Human Myeloid Dendritic Cells Leads to a Th1 Response in CD4⁺T Cells from Healthy Donors and Patients with Kala‐Azar