TLR7 Sensing by Neutrophils Is Critical for the Control of Cutaneous Leishmaniasis.

Cell Reports
Ivo B RegliFabienne Tacchini-Cottier

Abstract

Neutrophils are rapidly recruited to sites of infection, where they kill invading pathogens. However, they may also act as early temporary shelters, favoring subsequent pathogen dissemination in the host. We find that TLR7 sensing of the protozoan Leishmania parasite in neutrophils is essential for early parasite load regulation. Neutrophil effector functions, including reactive oxygen species (ROS) and neutrophil extracellular trap formation, are decreased in the absence of TLR7, resulting in higher parasite load and selective parasite replication in Tlr7-/- neutrophils. Leishmania-infected Tlr7-/- mice develop a chronic unhealing lesion, despite Th1 cell differentiation, and we show that Tlr7-/- neutrophils alone mediate this effect. Conversely, topical treatment with a TLR7 agonist early in infection induces smaller lesion development than in untreated mice. Collectively, these findings highlight that parasite TLR7 triggering in neutrophils regulates early innate functions with major consequences on subsequent disease evolution, opening avenues for possible treatment strategies.

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Citations

Jan 16, 2021·Biochemical Society Transactions·Thalia Pacheco-FernandezAbhay R Satoskar
Mar 19, 2021·Frontiers in Immunology·Katiuska PasselliFabienne Tacchini-Cottier
Oct 26, 2021·Frontiers in Cellular and Infection Microbiology·Yuanfa FengJun Huang
Jan 19, 2022·PLoS Pathogens·Katiuska PasselliFabienne Tacchini-Cottier

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