{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,5]],"date-time":"2026-11-05T15:46:27Z","timestamp":1793893587523,"version":"4.8.0"},"reference-count":58,"publisher":"Rockefeller University Press","issue":"1","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2014,1,13]]},"abstract":"<jats:p>IL-17A\u2013expressing CD4+ T cells (Th17 cells) are generally regarded as key effectors of autoimmune inflammation. However, not all Th17 cells are pro-inflammatory. Pathogenic Th17 cells that induce autoimmunity in mice are distinguished from nonpathogenic Th17 cells by a unique transcriptional signature, including high Il23r expression, and these cells require Il23r for their inflammatory function. In contrast, defining features of human pro-inflammatory Th17 cells are unknown. We show that pro-inflammatory human Th17 cells are restricted to a subset of CCR6+CXCR3hiCCR4loCCR10\u2212CD161+ cells that transiently express c-Kit and stably express P-glycoprotein (P-gp)\/multi-drug resistance type 1 (MDR1). In contrast to MDR1\u2212 Th1 or Th17 cells, MDR1+ Th17 cells produce both Th17 (IL-17A, IL-17F, and IL-22) and Th1 (IFN-\u03b3) cytokines upon TCR stimulation and do not express IL-10 or other anti-inflammatory molecules. These cells also display a transcriptional signature akin to pathogenic mouse Th17 cells and show heightened functional responses to IL-23 stimulation. In vivo, MDR1+ Th17 cells are enriched and activated in the gut of Crohn\u2019s disease patients. Furthermore, MDR1+ Th17 cells are refractory to several glucocorticoids used to treat clinical autoimmune disease. Thus, MDR1+ Th17 cells may be important mediators of chronic inflammation, particularly in clinical settings of steroid resistant inflammatory disease.<\/jats:p>","DOI":"10.1084\/jem.20130301","type":"journal-article","created":{"date-parts":[[2014,1,7]],"date-time":"2014-01-07T04:15:02Z","timestamp":1389068102000},"page":"89-104","update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":437,"title":["Pro-inflammatory human Th17 cells selectively express P-glycoprotein and are refractory to glucocorticoids"],"prefix":"10.1084","volume":"211","author":[{"given":"Radha","family":"Ramesh","sequence":"first","affiliation":[{"name":"Tempero Pharmaceuticals, Inc., 200 Technology Square, Suite 602, Cambridge, MA 02139 1"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lina","family":"Kozhaya","sequence":"additional","affiliation":[{"name":"Department of Microbiology, New York University School of Medicine, New York, NY 10016 2"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kelly","family":"McKevitt","sequence":"additional","affiliation":[{"name":"Department of Cancer Biology, The Scripps Research Institute, Jupiter, FL 33458 3"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ivana M.","family":"Djuretic","sequence":"additional","affiliation":[{"name":"Tempero Pharmaceuticals, Inc., 200 Technology Square, Suite 602, Cambridge, MA 02139 1"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thaddeus J.","family":"Carlson","sequence":"additional","affiliation":[{"name":"Tempero Pharmaceuticals, Inc., 200 Technology Square, Suite 602, Cambridge, MA 02139 1"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maria A.","family":"Quintero","sequence":"additional","affiliation":[{"name":"John P. 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