Protective immune response mediated by neutrophils in experimental visceral leishmaniasis is enhanced by IL-32γ
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2022
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Neutrophils are important cells in protection against microbial infections including visceral leishmaniasis (VL). It
is well known that IL-32γ increases the protective T helper 17 cell mediated immune response against Leishmania
infantum. Thus, in this study we evaluated whether IL-32 γ can increase the protective role of neutrophils against
VL. In comparison with wild type (WT) mice, transgenic mice for human IL-32 γ (IL-32 γ Tg) presented a higher
frequency and absolute number of neutrophils in both spleen and liver after the establishment of L. infantum
infection. The IL-32 concentrations correlated with neutrophil numbers in the infected tissues. The IL-32 γ
-induced recruitment of neutrophils was dependent on IL-17, since inhibition of Th17 T cells generation and IL-
17 production with digoxin treatment reversed the effects of IL-32 γ. In murine neutrophils, the presence of IL-32
γ enhanced the phagocytosis of L. infantum via CR3. In addition, murine IL-32 γ Tg neutrophils were able to kill
L. infantum due to the increased production of ROS when compared with WT neutrophils. In fact, IL-32 γ Tg mice
lost their ability to control infection by L. infantum when neutrophils were depleted. In parallel, treatment of
human neutrophils with recombinant IL-32 γ increased phagocytosis and ROS-dependent killing of L. infantum,
similarly to murine IL-32 γ Tg neutrophils. The data show that IL-32 γ induces neutrophil recruitment to organs
affected by VL and increases phagocytosis and killing of L. infantum by neutrophils. Together, data indicate the
pivotal axis IL-32 γ -Th17-neutrophils to control VL.
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Visceral leishmaniasis, Leishmania infantum, Neutrophils, IL-32, Immune response
Citação
GOMES, Rodrigo Saar et al. Protective immune response mediated by neutrophils in experimental visceral leishmaniasis is enhanced by IL-32γ. Cellular Immunology, New York, v. 371, e104449, 2022. DOI: 10.1016/j.cellimm.2021.104449. Disponível em: https://www.sciencedirect.com/science/article/pii/S0008874921001684?via%3Dihub. Acesso em: 19 mar. 2025.