Abstract
Interleukin-32 (IL-32) has several immune regulatory properties, which have driven its investigation in the context of various diseases. IL-32 expression is reported to be induced in the lesions of patients with American tegumentary leishmaniasis (ATL) by the New World Leishmania spp. that are responsible for causing ATL and visceral leishmaniasis (VL). IL-32 expression may elevate the inflammatory process through the induction of pro-inflammatory cytokines and also via mechanisms directed to kill the parasites. The genetic variants of IL-32 might be associated with the resistance or susceptibility to ATL, while different isoforms of IL-32 could be associated with distinct T helper lymphocyte profiles. IL-32 also determines the transcriptional profile in the bone marrow progenitor cells to mediate the trained immunity induced by β-glucan and BCG, thereby contributing to the resistance against Leishmania. IL-32γ is essential for the vitamin D-dependent microbicidal pathway for parasite control. In this context, the present review report briefly discusses the data retrieved from the studies conducted on IL-32 in leishmaniasis in humans and mice to highlight the current challenges to understanding the role of IL-32 in leishmaniasis.
Highlights
Interleukin 32 (IL-32) [1], which was previously known as the Natural Killer (NK) cell transcript 4 (NK4), is a cytokine secreted by both immune and non-immune cells
The IL-1 receptor antagonist (IL-1Ra) mRNA and protein levels and IL-10 mRNA levels were higher after exposure to L. amazonensis compared to L. braziliensis, and only L. amazonensis-induced IL-1Ra was affected by IL-32g expression [10]. These findings suggested that the effect of IL32g expression on cytokine production differs with the Leishmania species
The stratification of healthy individuals according to their IL32 single-nucleotide polymorphism (SNP) rs4786370 genotype (200FG cohort; 79) revealed that the CC genotype expressed higher levels of IL-32g, IL-1b, IL-6, and TNF-a in b-glucan-trained macrophages compared to the TT genotype
Summary
Laboratorio de Imunidade Natural, Instituto de Patologia Tropical e Saude Publica, Universidade Federal de Goias, Goiania, Brazil. Interleukin-32 (IL-32) has several immune regulatory properties, which have driven its investigation in the context of various diseases. IL-32 expression is reported to be induced in the lesions of patients with American tegumentary leishmaniasis (ATL) by the New World Leishmania spp. that are responsible for causing ATL and visceral leishmaniasis (VL). IL-32 determines the transcriptional profile in the bone marrow progenitor cells to mediate the trained immunity induced by b-glucan and BCG, thereby contributing to the resistance against Leishmania. IL-32g is essential for the vitamin D-dependent microbicidal pathway for parasite control. In this context, the present review report briefly discusses the data retrieved from the studies conducted on IL-32 in leishmaniasis in humans and mice to highlight the current challenges to understanding the role of IL-32 in leishmaniasis
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