Abstract
IL-27 is a cytokine that exerts diverse effects on the cells of innate and adaptive immune systems. Chiefly expressed in macrophages and dendritic cells during the early phase of Leishmania infection, IL-27 contributes to the protection against L. major infection but suppresses the protective Th1 response against L. donovani, L. infantum, L. amazonensis and L. braziliensis infections, suggesting its functional duality. During the late stage of Leishmania infection, IL-27 limits the immunopathogenic reactions and tissue damages. Herein, we analyze the mechanism of the functional duality of IL-27 in the resistance or susceptibility to Leishmania infection, prompting IL-27 for anti-Leishmanial therapy.
Highlights
IL-27 is a heterodimer of p28 and Epstein-Barr virus-induced gene 3 (EBI3) subunits and signals through IL-27-receptor complex, a heterodimer of IL-27Rα WSX-1 and gp130 subunits [1]
PBMC cultures from patients with cutaneous Leishmaniasis (CL) and mucocutaneous Leishmaniasis (MCL) when supplemented with IL-27 do not show any change in the production of IL10 [81]. These findings indicate that the cytokine-producing cells from patients with CL and MCL are unresponsive to the regulatory effects of IL-27
IL-27 signaling contributes to the Th1 cell-related protective response in the L. major-infected mice, the same pathway may enhance the susceptibility to L. amazonensis, perhaps due to the differences in protein kinase R (PKR)-mediated signaling between L. major- and L. amazonensis-infected macrophages
Summary
IL-27 is a heterodimer of p28 and Epstein-Barr virus-induced gene 3 (EBI3) subunits and signals through IL-27-receptor complex, a heterodimer of IL-27Rα WSX-1 and gp130 subunits [1]. The increased susceptibility of WSX-1−/− mice to L. major is accompanied by the Leishmania-induced IL-4 production initially; blockade of IL-4 during the initial phase of infection abolishes the early requirement for IL-27 for the development of effective anti-parasitic responses.
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