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. 2012 Aug 14:3:251.
doi: 10.3389/fimmu.2012.00251. eCollection 2012.

Immunobiology of visceral leishmaniasis

Affiliations

Immunobiology of visceral leishmaniasis

Rajiv Kumar et al. Front Immunol. .

Abstract

Visceral leishmaniasis (VL), commonly known as kala-azar, is caused by Leishmania donovani and Leishmania infantum (Leishmania chagasi in the Americas). These Leishmania species infect macrophages throughout the viscera, and parasites are typically found in the spleen, liver, and bone marrow. Patients with active disease typically exhibit marked immunosuppression, lack reactivity to the Leishmania skin test (LST), a delayed type hypersensitivity test, and their peripheral blood mononuclear cells (PBMC) fail to respond when stimulated with leishmanial antigens in vitro. However, most people infected with visceralizing species of Leishmania never develop disease. Understanding immune failure and the underlying immune mechanism that lead to disease as well as control of infection are key questions for research in this field. In this review, we discuss immunological events described in human and experimental VL and how these can affect the outcome of infection.

Keywords: IL-10; Leishmania donovani; T cells; immune regulation; visceral leishmaniasis.

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Figures

FIGURE 1
FIGURE 1
Regulatory feedback loop facilitate parasite persistence. (1) Activated T cells both CD4 and CD8 produce IFNγ, which in combination with IL-1β drives IL-27 production by macrophages. (2a) IL-27 inhibits generation of potentially protective Th17 cells and (2b) promotes together with IL-21 the generation IL-10 secreting T cells. (3) IL-10 cause down-regulation of IL-12, MHC class II as well as co-stimulatory molecules on macrophages and render macrophage unresponsive to activation signals such as IFNγ. Together this facilitates parasite replication and disease progression.

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