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Immune responses in the lung are important to restrict the growth of M. tuberculosis to prevent the development of disease.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>To investigate innate and adaptive immune responses to M. tuberculosis in bronchoalveolar lavage from HIV-1\u2013infected persons without active tuberculosis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Peripheral blood was drawn and bronchoalveolar lavage (BAL) performed on healthy, HIV-1\u2013uninfected (n = 21) and HIV-1\u2013infected (n = 15) adults. Growth of M. tuberculosis was assessed in monocytes and alveolar macrophages. Cytokine expression by mycobacteria-specific CD4 and CD8 T cells was measured by intracellular cytokine staining or IFN-\u03b3 ELISpot.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Measurements and Main Results<\/jats:title>\n                    <jats:p>Mycobacterial growth in monocytes or alveolar macrophages from HIV-1\u2013infected and \u2013uninfected persons did not differ. Total CD4 T-cell frequencies in BAL were lower in HIV-1\u2013infected than in HIV-1\u2013uninfected persons (P &amp;lt; 0.001). Mycobacteria (bacillus Calmette-Gu\u00e9rin)-specific CD4 T-cell responses in BAL were severely impaired: Frequencies of cells expressing IFN-\u03b3 or tumor necrosis factor (TNF)-\u03b1, as well as polyfunctional cells, expressing IFN-\u03b3, TNF-\u03b1, and IL-2 together, were lower in HIV-1\u2013infected persons than in uninfected controls (P &amp;lt; 0.01 for all).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>In addition to a total CD4 T-cell deficit, the function of mycobacteria-specific CD4 T cells is significantly impaired in the lung of HIV-1\u2013infected persons, which may account for the HIV-1\u2013associated elevated risk for developing tuberculosis.<\/jats:p>\n                  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