| First Author | Bohrer AC | Year | 2018 |
| Journal | J Immunol | Volume | 201 |
| Issue | 6 | Pages | 1645-1650 |
| PubMed ID | 30068597 | Mgi Jnum | J:265209 |
| Mgi Id | MGI:6199393 | Doi | 10.4049/jimmunol.1800438 |
| Citation | Bohrer AC, et al. (2018) Cutting Edge: IL-1R1 Mediates Host Resistance to Mycobacterium tuberculosis by Trans-Protection of Infected Cells. J Immunol 201(6):1645-1650 |
| abstractText | 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 was provided to infected cells in trans by both nonhematopoietic and hematopoietic cells. Thus, IL-1R1-mediated host resistance to M. tuberculosis infection does not involve mechanisms of cell-autonomous antimicrobicidal effector functions in phagocytes but requires the cooperation between infected cells and other cells of hematopoietic or nonhematopoietic origin to promote bacterial containment and control of infection. |
