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, 2 (2), 135-46

Immunological Perspectives of Leishmaniasis

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Immunological Perspectives of Leishmaniasis

Susanne Nylén et al. J Glob Infect Dis.

Abstract

Leishmania parasites have been widely used in experimental models to understand generation, maintenance and failure of immune responses underlying resistance and susceptibility to infection. The clinical outcomes of Leishmania infection depend on the infecting species and the immune status of the host. Noticeably most people exposed Leishmania never develop overt disease. Understanding the immunological events that result in failure or successful control of the parasites is fundamental to both design and evaluation of vaccines and therapies against the leishmaniases. Recent studies visualizing immune response to Leishmania major in the skin have given new insights into the different immune cells acting as hosts the parasite during different stage of infection. Control of Leishmania infection and disease progression has been associated with generation of T-helper (Th) 1 and Th2 responses respectively. Though still valid in several aspects, the Th1/Th2 paradigm is an oversimplification in need of revision. Th2 polarization has never explained severity of human leishmanial disease and a number of other T-cell subsets, including regulatory T- and Th17- cells, have important roles in susceptibility and resistance of both experimental and human leishmanial disease. This review gives an updated overview of immunological response considered to be of importance in protection, susceptibility, disease progression and cure of leishmaniasis, with a special emphasis on human diseases.

Keywords: Apoptosis; Human; Immunology; Innate immunity; Leishmania; T cells; Vaccine.

Conflict of interest statement

Conflict of Interest: None declared.

Figures

Figure 1
Figure 1
Apoptosis - a way to avoid immune activation and promote survival; a) Sandflies inject apoptotic parasites together with viable. Apoptotic promastigotes facilitate infection and prevent activation of neutrophils (PMN).[108109]; b) Parasites delay neutrophil apoptosis, giving monocytes/macrophages (Mφ) time to enter the site of infection; c) Silent entry of parasite into macrophages via apoptotic neutrophils.[12]; d) Viable amastigotes expose PS and mimic apoptotic cells. This facilitates internalization and increases macrophage susceptibility to leishmanial growth[25]

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