{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,31]],"date-time":"2026-08-31T02:02:39Z","timestamp":1788141759749,"version":"build-2803163510"},"reference-count":36,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2015,7,6]],"date-time":"2015-07-06T00:00:00Z","timestamp":1436140800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"Division of Intramural Research, NIAID, NIH"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Immunology"],"published-print":{"date-parts":[[2015,10]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>The immune system plays an important role in the pathogenesis of pulmonary tuberculosis\u2013type 2 diabetes mellitus (<jats:styled-content style=\"fixed-case\">PTB<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">DM<\/jats:styled-content>) co\u2010morbidity. However, the phenotypic profile of leucocyte subsets at homeostasis in individuals with active or latent tuberculosis (<jats:styled-content style=\"fixed-case\">LTB<\/jats:styled-content>) with coincident diabetes is not known. To characterize the influence of diabetes on leucocyte phenotypes in <jats:styled-content style=\"fixed-case\">PTB<\/jats:styled-content> or <jats:styled-content style=\"fixed-case\">LTB<\/jats:styled-content>, we examined the frequency (<jats:italic>F<\/jats:italic><jats:sub>o<\/jats:sub>) of leucocyte subsets in individuals with <jats:styled-content style=\"fixed-case\">TB<\/jats:styled-content> with (<jats:styled-content style=\"fixed-case\">PTB<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">DM<\/jats:styled-content>) or without (<jats:styled-content style=\"fixed-case\">PTB<\/jats:styled-content>) diabetes; individuals with latent <jats:styled-content style=\"fixed-case\">TB<\/jats:styled-content> with (<jats:styled-content style=\"fixed-case\">LTB<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">DM<\/jats:styled-content>) or without (<jats:styled-content style=\"fixed-case\">LTB<\/jats:styled-content>) diabetes and non\u2010<jats:styled-content style=\"fixed-case\">TB<\/jats:styled-content>\u2010infected individuals with (<jats:styled-content style=\"fixed-case\">NTB<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">DM<\/jats:styled-content>) or without (<jats:styled-content style=\"fixed-case\">NTB<\/jats:styled-content>) diabetes. Coincident <jats:styled-content style=\"fixed-case\">DM<\/jats:styled-content> is characterized by significantly lower <jats:italic>F<\/jats:italic><jats:sub>o<\/jats:sub> of effector memory <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>4<jats:sup>+<\/jats:sup> T cells in <jats:styled-content style=\"fixed-case\">LTB<\/jats:styled-content> individuals. In contrast, <jats:styled-content style=\"fixed-case\">DM<\/jats:styled-content> is characterized by significantly lower <jats:italic>F<\/jats:italic><jats:sub>o<\/jats:sub> of effector memory <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>8<jats:sup>+<\/jats:sup> T cells and significantly higher <jats:italic>F<\/jats:italic><jats:sub>o<\/jats:sub> of central memory <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>8<jats:sup>+<\/jats:sup> T cells in <jats:styled-content style=\"fixed-case\">PTB<\/jats:styled-content> individuals. Coincident <jats:styled-content style=\"fixed-case\">DM<\/jats:styled-content> resulted in significantly higher <jats:italic>F<\/jats:italic><jats:sub>o<\/jats:sub> of classical memory B cells in <jats:styled-content style=\"fixed-case\">PTB<\/jats:styled-content> and significantly higher <jats:italic>F<\/jats:italic><jats:sub>o<\/jats:sub> of activated memory and atypical B cells in <jats:styled-content style=\"fixed-case\">LTB<\/jats:styled-content> individuals. Coincident <jats:styled-content style=\"fixed-case\">DM<\/jats:styled-content> resulted in significantly lower <jats:italic>F<\/jats:italic><jats:sub>o<\/jats:sub> of classical and intermediate monocytes in <jats:styled-content style=\"fixed-case\">PTB<\/jats:styled-content>,<jats:styled-content style=\"fixed-case\"> LTB<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">NTB<\/jats:styled-content> individuals. Finally, <jats:styled-content style=\"fixed-case\">DM<\/jats:styled-content> resulted in significantly lower <jats:italic>F<\/jats:italic><jats:sub>o<\/jats:sub> of myeloid and plasmacytoid dendritic cells in <jats:styled-content style=\"fixed-case\">PTB<\/jats:styled-content>,<jats:styled-content style=\"fixed-case\"> LTB<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">NTB<\/jats:styled-content> individuals. Our data reveal that coincident diabetes alters the cellular subset distribution of T cells, B cells, dendritic cells and monocytes in both individuals with active <jats:styled-content style=\"fixed-case\">TB<\/jats:styled-content> and those with latent <jats:styled-content style=\"fixed-case\">TB<\/jats:styled-content>, thus potentially impacting the pathogenesis of this co\u2010morbid condition.<\/jats:p>","DOI":"10.1111\/imm.12496","type":"journal-article","created":{"date-parts":[[2015,6,19]],"date-time":"2015-06-19T17:18:39Z","timestamp":1434734319000},"page":"243-250","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":36,"title":["Profiling leucocyte subsets in tuberculosis\u2013diabetes co\u2010morbidity"],"prefix":"10.1111","volume":"146","author":[{"given":"Nathella Pavan","family":"Kumar","sequence":"first","affiliation":[{"name":"National Institutes of Health\u2014NIRT\u2014International Centre for Excellence in Research Chennai India"},{"name":"National Institute for Research in Tuberculosis Chennai India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kadar","family":"Moideen","sequence":"additional","affiliation":[{"name":"National Institutes of Health\u2014NIRT\u2014International Centre for Excellence in Research Chennai India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sharmila D.","family":"Dhakshinraj","sequence":"additional","affiliation":[{"name":"National Institutes of Health\u2014NIRT\u2014International Centre for Excellence in Research Chennai India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vaithilingam V.","family":"Banurekha","sequence":"additional","affiliation":[{"name":"National Institute for Research in Tuberculosis Chennai India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dina","family":"Nair","sequence":"additional","affiliation":[{"name":"National Institute for Research in Tuberculosis Chennai India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chandrakumar","family":"Dolla","sequence":"additional","affiliation":[{"name":"National Institute for Research in Tuberculosis Chennai India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul","family":"Kumaran","sequence":"additional","affiliation":[{"name":"National Institute for Research in Tuberculosis Chennai India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Subash","family":"Babu","sequence":"additional","affiliation":[{"name":"National Institutes of Health\u2014NIRT\u2014International Centre for Excellence in Research Chennai India"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2015,7,6]]},"reference":[{"key":"e_1_2_8_2_1","unstructured":"WHO. 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