| First Author | Segueni N | Year | 2016 |
| Journal | Sci Rep | Volume | 6 |
| Pages | 22454 | PubMed ID | 26931771 |
| Mgi Jnum | J:259972 | Mgi Id | MGI:6102089 |
| Doi | 10.1038/srep22454 | Citation | Segueni N, et al. (2016) Innate myeloid cell TNFR1 mediates first line defence against primary Mycobacterium tuberculosis infection. Sci Rep 6:22454 |
| abstractText | TNF is crucial for controlling Mycobacterium tuberculosis infection and understanding how will help immunomodulating the host response. Here we assessed the contribution of TNFR1 pathway from innate myeloid versus T cells. We first established the prominent role of TNFR1 in haematopoietic cells for controlling M. tuberculosis in TNFR1 KO chimera mice. Further, absence of TNFR1 specifically on myeloid cells (M-TNFR1 KO) recapitulated the uncontrolled M. tuberculosis infection seen in fully TNFR1 deficient mice, with increased bacterial burden, exacerbated lung inflammation, and rapid death. Pulmonary IL-12p40 over-expression was attributed to a prominent CD11b(+) Gr1(high) cell population in infected M-TNFR1 KO mice. By contrast, absence of TNFR1 on T-cells did not compromise the control of M. tuberculosis infection over 6-months. Thus, the protective TNF/TNFR1 pathway essential for controlling primary M. tuberculosis infection depends on innate macrophage and neutrophil myeloid cells, while TNFR1 pathway in T cells is dispensable. |
