Cutting Edge: IL-1R1 Mediates Host Resistance to Mycobacterium tuberculosis by Trans-Protection of Infected Cells.

ABSTRACT: IL-1R1 deficiency in mice causes severe susceptibility to Mycobacterium tuberculosis Mice and macrophage cultures lacking IL-1R1 display increased bacterial growth, suggesting that phagocytes may require IL-1R1-dependent antimicrobial signals to limit intracellular M. tuberculosis replication directly. However, the myeloid-cell-intrinsic versus -extrinsic requirements for IL-1R1 to control M. tuberculosis infection in mice have not been directly addressed. Using single-cell analysis of infected cells, competitive mixed bone marrow chimeras, and IL-1R1 conditional mutant mice, we show in this article that IL-1R1 expression by pulmonary phagocytes is uncoupled from their ability to control intracellular M. tuberculosis growth. Importantly, IL-1R1-dependent control

SUBMITTER: Bohrer AC 

PROVIDER: S-EPMC6125209 | biostudies-literature | 2018 Sep

REPOSITORIES: biostudies-literature