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Despite self-reliant rescue from infection, BCG vaccination, and treatment, long-term memory is rarely established against <jats:italic>Mycobacterium tuberculosis<\/jats:italic> (<jats:italic>M<\/jats:italic>.<jats:italic>tb<\/jats:italic>) resulting in recurrent tuberculosis (TB). Here, we show that berberine (BBR) enhances innate defense mechanisms against <jats:italic>M<\/jats:italic>.<jats:italic>tb<\/jats:italic> and stimulates the differentiation of Th1\/Th17 specific effector memory (T<jats:sub>EM<\/jats:sub>), central memory (T<jats:sub>CM<\/jats:sub>), and tissue-resident memory (T<jats:sub>RM<\/jats:sub>) responses leading to enhanced host protection against drug-sensitive and drug-resistant TB. Through whole proteome analysis of human PBMCs derived from PPD<jats:sup>+<\/jats:sup> healthy individuals, we identify BBR modulated NOTCH3\/PTEN\/AKT\/FOXO1 pathway as the central mechanism of elevated T<jats:sub>EM<\/jats:sub> and T<jats:sub>RM<\/jats:sub> responses in the human CD4<jats:sup>+<\/jats:sup> T cells. Moreover, BBR-induced glycolysis resulted in enhanced effector functions leading to superior Th1\/Th17 responses in human and murine T cells. This regulation of T cell memory by BBR remarkably enhanced the BCG-induced anti-tubercular immunity and lowered the rate of TB recurrence due to relapse and re-infection. These results thus suggest tuning immunological memory as a feasible approach to augment host resistance against TB and unveil BBR as a potential adjunct immunotherapeutic and immunoprophylactic against TB.<\/jats:p>","DOI":"10.1371\/journal.ppat.1011165","type":"journal-article","created":{"date-parts":[[2023,3,7]],"date-time":"2023-03-07T18:31:13Z","timestamp":1678213873000},"page":"e1011165","update-policy":"https:\/\/doi.org\/10.1371\/journal.ppat.corrections_policy","source":"Crossref","is-referenced-by-count":28,"title":["Berberine governs NOTCH3\/AKT signaling to enrich lung-resident memory T cells during 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