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By characterizing Mtb infection in mouse strains that model the genetic heterogeneity of an outbred population, we identified strains that control Mtb comparably to a standard IFN\u03b3-dependent mouse model but with substantially lower lung IFN\u03b3 levels. We report that these mice have a significantly altered CD4 T cell profile that specifically lacks the terminal effector Th1 subset and that this phenotype is detectable before infection. These mice still require T cells to control bacterial burden but are less dependent on IFN\u03b3 signaling. Instead, noncanonical immune features such as Th17-like CD4 and \u03b3\u03b4T cells correlate with low bacterial burden. 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