{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T16:54:42Z","timestamp":1791219282683,"version":"4.1.0"},"reference-count":49,"publisher":"American Society for Microbiology","issue":"6","license":[{"start":{"date-parts":[[2012,6,1]],"date-time":"2012-06-01T00:00:00Z","timestamp":1338508800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2012,6]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            Natural killer T (NKT) cells are known to play a protective role in the immune responses of mice against a variety of infectious pathogens. However, little is known about the detailed information of NKT cells in patients with\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Mycobacterium tuberculosis<\/jats:named-content>\n            infection. The aims of this study were to examine NKT cell levels and functions in patients with active\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">M. tuberculosis<\/jats:named-content>\n            infection, to investigate relationships between NKT cell levels and clinical parameters, and to determine the mechanism responsible for the poor response to \u03b1-galactosylceramide (\u03b1-GalCer). NKT cell levels were significantly lower in the peripheral blood of pulmonary tuberculosis and extrapulmonary tuberculosis patients, and the proliferative responses of NKT cells to \u03b1-GalCer were also lower in patients, whereas NKT cell levels and responses were comparable in latent tuberculosis infection subjects and healthy controls. Furthermore, this NKT cell deficiency was found to be correlated with serum C-reactive protein levels. In addition, the poor response to \u03b1-GalCer in\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">M. tuberculosis<\/jats:named-content>\n            -infected patients was found to be due to increased NKT cell apoptosis, reduced CD1d expression, and a defect in NKT cells. Notably,\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">M. tuberculosis<\/jats:named-content>\n            infection was associated with an elevated expression of the inhibitory programmed death-1 (PD-1) receptor on NKT cells, and blockade of PD-1 signaling enhanced the response to \u03b1-GalCer. This study shows that NKT cell levels and functions are reduced in\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">M. tuberculosis<\/jats:named-content>\n            -infected patients and these deficiencies were found to reflect the presence of active tuberculosis.\n          <\/jats:p>","DOI":"10.1128\/iai.06018-11","type":"journal-article","created":{"date-parts":[[2012,3,13]],"date-time":"2012-03-13T04:50:05Z","timestamp":1331614205000},"page":"2100-2108","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":77,"title":["Dysfunction of Natural Killer T Cells in Patients with Active Mycobacterium tuberculosis Infection"],"prefix":"10.1128","volume":"80","author":[{"given":"Seung-Jung","family":"Kee","sequence":"first","affiliation":[{"name":"Department of Laboratory Medicine, Chonnam National University Medical School and Hospital, Gwangju, Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yong-Soo","family":"Kwon","sequence":"additional","affiliation":[{"name":"Department of Pulmonary and Critical Care Medicine, Chonnam National University Medical School and Hospital, Gwangju, Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yong-Wook","family":"Park","sequence":"additional","affiliation":[{"name":"Department of Rheumatology, Research Institute of Medical Sciences, Brain Korea 21, Chonnam National University Medical School and Hospital, Gwangju, Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Young-Nan","family":"Cho","sequence":"additional","affiliation":[{"name":"Department of Rheumatology, Research Institute of Medical Sciences, Brain Korea 21, Chonnam National University Medical School and Hospital, Gwangju, Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sung-Ji","family":"Lee","sequence":"additional","affiliation":[{"name":"Department of Rheumatology, Research Institute of Medical Sciences, Brain Korea 21, Chonnam National University Medical School and Hospital, Gwangju, Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tae-Jong","family":"Kim","sequence":"additional","affiliation":[{"name":"Department of Rheumatology, Research Institute of Medical Sciences, Brain Korea 21, Chonnam National University Medical School and Hospital, Gwangju, Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shin-Seok","family":"Lee","sequence":"additional","affiliation":[{"name":"Department of Rheumatology, Research Institute of Medical Sciences, Brain Korea 21, Chonnam National University Medical School and Hospital, Gwangju, Republic of 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