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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.

Innate myeloid cell TNFR1 mediates first line defence against primary Mycobacterium tuberculosis infection.