{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T05:29:27Z","timestamp":1791091767900,"version":"4.1.0"},"reference-count":54,"publisher":"Oxford University Press (OUP)","issue":"10","license":[{"start":{"date-parts":[[2006,11,1]],"date-time":"2006-11-01T00:00:00Z","timestamp":1162339200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2006,11,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Although it is known that IFN-\u03b3-secreting T cells are critical for control of Mycobacterium tuberculosis infection, the contribution of IFN-\u03b3 produced by NK cells to host resistance to the pathogen is less well understood. By using T cell-deficient RAG\u2212\/\u2212 mice, we showed that M. tuberculosis stimulates NK cell-dependent IFN-\u03b3 production in naive splenic cultures and in lungs of infected animals. More importantly, common cytokine receptor \u03b3-chain\u2212\/\u2212RAG\u2212\/\u2212 animals deficient in NK cells, p40\u2212\/\u2212RAG\u2212\/\u2212, or anti-IFN-\u03b3 mAb-treated RAG\u2212\/\u2212 mice displayed significantly increased susceptibility to M. tuberculosis infection compared with untreated NK-sufficient RAG\u2212\/\u2212 controls. Studies comparing IL-12 p40- and p35-deficient RAG\u2212\/\u2212 mice indicated that IL-12 plays a more critical role in the induction of IFN-\u03b3-mediated antimycobacterial effector functions than IL-23 or other p40-containing IL-12 family members. The increased susceptibility of IL-12-deficient or anti-IFN-\u03b3 mAb-treated RAG\u2212\/\u2212 mice was associated not only with elevated bacterial loads, but also with the development of granulocyte-enriched foci in lungs. This tissue response correlated with increased expression of the granulocyte chemotactic chemokines KC and MIP-2 in NK as well as other leukocyte populations. Interestingly, depletion of granulocytes further increased bacterial burdens and exacerbated pulmonary pathology in these animals, revealing a compensatory function for neutrophils in the absence of IFN-\u03b3. The above observations indicate that NK cell-derived IFN-\u03b3 differentially regulates T-independent resistance and granulocyte function in M. tuberculosis infection and suggest that this response could serve as an important barrier in AIDS patients or other individuals with compromised CD4+ T cell function.<\/jats:p>","DOI":"10.4049\/jimmunol.177.10.7086","type":"journal-article","created":{"date-parts":[[2014,4,18]],"date-time":"2014-04-18T19:39:04Z","timestamp":1397849944000},"page":"7086-7093","source":"Crossref","is-referenced-by-count":197,"title":["NK Cell-Derived IFN-\u03b3 Differentially Regulates Innate Resistance and Neutrophil Response in T Cell-Deficient Hosts Infected with\n                    <i>Mycobacterium tuberculosis<\/i>"],"prefix":"10.1093","volume":"177","author":[{"given":"Carl G","family":"Feng","sequence":"first","affiliation":[{"name":"Immunobiology Section, National Institute of Allergy and Infectious Diseases , Bethesda, MD 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mallika","family":"Kaviratne","sequence":"additional","affiliation":[{"name":"Immunopathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases , Bethesda, MD 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Antonio Gigliotti","family":"Rothfuchs","sequence":"additional","affiliation":[{"name":"Immunobiology Section, National Institute of Allergy and Infectious Diseases , Bethesda, MD 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Allen","family":"Cheever","sequence":"additional","affiliation":[{"name":"Biomedical Research Institute , Rockville, MD 20852"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sara","family":"Hieny","sequence":"additional","affiliation":[{"name":"Immunobiology Section, National Institute of Allergy and Infectious Diseases , Bethesda, MD 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Howard A","family":"Young","sequence":"additional","affiliation":[{"name":"Laboratory of Experimental Immunology, National Cancer Institute, Center for Cancer Research , Frederick, MD 21702"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas A","family":"Wynn","sequence":"additional","affiliation":[{"name":"Immunopathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases , Bethesda, MD 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alan","family":"Sher","sequence":"additional","affiliation":[{"name":"Immunobiology Section, National Institute of Allergy and Infectious Diseases , Bethesda, MD 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2006,11,15]]},"reference":[{"key":"2026020214064631200_R1","first-page":"93","volume-title":"Annu. 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