Leptin is a pleiotropic hormone proposed to link nutritional status to the development of strong Th1 immunity. As Mycobacterium tuberculosis (MTb) control is affected by starvation and diabetes, we studied the role of the leptin receptor in regulating distinct immune cells during chronic infection. Infected db/db mice, bearing a natural mutation in the leptin receptor, have a markedly increased bacterial load in their lungs when compared to their wild-type (WT) counterparts. In response to MTb infection, db/db mice exhibited disorganized granulomas, neutrophilia, and reduced B cell migration to the lungs, correlating with dysfunctional lung chemokine responses that include XCL1, CCL2, CXCL1, CXCL2, and CXCL13. In a db/db lung, myeloid cells were delayed in their production of inducible nitric oxide synthase (iNOS) and had reduced expression of MHC I and II. Although the Th1 cell response developed normally in the absence of leptin signaling, production of pulmonary IFNγ was delayed and ineffective. Surprisingly, a proper immune response took place in bone marrow (BM) chimeras lacking leptin receptor exclusively in BM-derived cells, indicating that leptin acts indirectly on immune cells to modulate the anti-tuberculosis response and bacterial control. Together these findings suggest that the pulmonary response to MTb is affected by the host’s nutritional status via the regulation of non-BM derived cells, and not through direct action of leptin on the Th1 immunity.