{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2024,6,13]],"date-time":"2024-06-13T23:17:50Z","timestamp":1718320670904},"reference-count":27,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2012,8,20]],"date-time":"2012-08-20T00:00:00Z","timestamp":1345420800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[2012,10]]},"abstract":"<jats:p>An inefficient <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>h1 response, coupled with skewed <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>h2 cytokine production, has been implicated to increase susceptibility to visceral leishmaniasis (<jats:styled-content style=\"fixed-case\">VL<\/jats:styled-content>) infection. The expression of the dipeptidyl peptidase <jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>d26 by polarized <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>h1 activates a chemokine cascade that recruits <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>h1 recruitment to the pathologic site. Here, we studied 42 patients with confirmed <jats:styled-content style=\"fixed-case\">VL<\/jats:styled-content> (mean age 24.80 \u00b1 16.26 years; range 3\u201370 years; 25 males and 17 females), 30 endemic controls, and 10 nonendemic controls. We observed a decrease in constitutive and antigen\u2010induced expression of <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>26 on the <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content> cells of <jats:styled-content style=\"fixed-case\">VL<\/jats:styled-content> patients. Soluble <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>26 (s<jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>26) levels in serum and <jats:styled-content style=\"fixed-case\">BM<\/jats:styled-content> were also found to be significantly lower in <jats:styled-content style=\"fixed-case\">VL<\/jats:styled-content> patients. Following successful therapy, increased s<jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>26 expression was observed. Tuberculosis pleural effusion derived <jats:styled-content style=\"fixed-case\">CCR<\/jats:styled-content>5<jats:sup>+<\/jats:sup><jats:styled-content style=\"fixed-case\">CXCR<\/jats:styled-content>3<jats:sup>+<\/jats:sup> effector <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content> cells showed enhanced chemokine\u2010driven migration in the presence of posttreatment <jats:styled-content style=\"fixed-case\">BM<\/jats:styled-content> aspirate containing high levels of s<jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>26. Moreover, <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\u2010cell migration could be inhibited by blocking <jats:styled-content style=\"fixed-case\">RANTES<\/jats:styled-content>, <jats:styled-content style=\"fixed-case\">IP<\/jats:styled-content>\u201010, and <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>26 signaling from the posttreatment aspirate with Ab. Our results indicate that, in <jats:styled-content style=\"fixed-case\">VL<\/jats:styled-content> patients, impaired expression and secretion of <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>26 compromises chemokine activation and thus <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\u2010cell recruitment, eventually resulting in a deficient state of local immunity at pathologic sites.<\/jats:p>","DOI":"10.1002\/eji.201141912","type":"journal-article","created":{"date-parts":[[2012,7,19]],"date-time":"2012-07-19T06:56:25Z","timestamp":1342680985000},"page":"2782-2791","source":"Crossref","is-referenced-by-count":11,"title":["Impaired expression of <scp>CD<\/scp>26 compromises <scp>T<\/scp>\u2010cell recruitment in human visceral leishmaniasis"],"prefix":"10.1002","volume":"42","author":[{"given":"Ambak K.","family":"Rai","sequence":"first","affiliation":[{"name":"Department of Transplant Immunology &amp; Immunogenetics AIIMS  New Delhi India"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Chandreshwar P.","family":"Thakur","sequence":"additional","affiliation":[{"name":"Balaji Utthan Sansthan  Patna Bihar India"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Prabin","family":"Kumar","sequence":"additional","affiliation":[{"name":"Department of Transplant Immunology &amp; Immunogenetics AIIMS  New Delhi India"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Dipendra K.","family":"Mitra","sequence":"additional","affiliation":[{"name":"Department of Transplant Immunology &amp; Immunogenetics AIIMS  New Delhi India"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2012,8,20]]},"reference":[{"key":"e_1_2_5_2_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.211439098"},{"key":"e_1_2_5_3_1","doi-asserted-by":"publisher","DOI":"10.2741\/2844"},{"key":"e_1_2_5_4_1","doi-asserted-by":"publisher","DOI":"10.1007\/0-306-47920-6_20"},{"key":"e_1_2_5_5_1","doi-asserted-by":"publisher","DOI":"10.1128\/MCB.25.17.7743-7757.2005"},{"key":"e_1_2_5_6_1","doi-asserted-by":"publisher","DOI":"10.1046\/j.1432-1327.2000.01634.x"},{"key":"e_1_2_5_7_1","doi-asserted-by":"crossref","first-page":"1714","DOI":"10.4049\/jimmunol.156.5.1714","article-title":"Serum high molecular weight dipeptidyl peptidase IV (CD26) is similar to a novel antigen DPPT\u2010L released from activated T cells","volume":"156","author":"Duke\u2010Cohan J. 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