Human CD26(high) T cells elicit tumor immunity against multiple malignancies via enhanced migration and persistence Journal Article

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Authors: Bailey, S. R.; Nelson, M. H.; Majchrzak, K.; Bowers, J. S.; Wyatt, M. M.; Smith, A. S.; Neal, L. R.; Shirai, K; Carpenito, C.; June, C. H.; Zilliox, M. J.; Paulos, C. M.
Article Title: Human CD26(high) T cells elicit tumor immunity against multiple malignancies via enhanced migration and persistence
Abstract: CD8(+) T lymphocytes mediate potent immune responses against tumor, but the role of human CD4(+) T cell subsets in cancer immunotherapy remains ill-defined. Herein, we exhibit that CD26 identifies three T helper subsets with distinct immunological properties in both healthy individuals and cancer patients. Although CD26(neg) T cells possess a regulatory phenotype, CD26(int) T cells are mainly naive and CD26(high) T cells appear terminally differentiated and exhausted. Paradoxically, CD26(high) T cells persist in and regress multiple solid tumors following adoptive cell transfer. Further analysis revealed that CD26(high) cells have a rich chemokine receptor profile (including CCR2 and CCR5), profound cytotoxicity (Granzyme B and CD107A), resistance to apoptosis (c-KIT and Bcl2), and enhanced stemness (beta-catenin and Lef1). These properties license CD26(high) T cells with a natural capacity to traffic to, regress and survive in solid tumors. Collectively, these findings identify CD4(+) T cell subsets with properties critical for improving cancer immunotherapy.
Journal Title: Nature communications
Volume: 8
Issue: 1
ISSN: 2041-1723; 2041-1723
Publisher: Unknown  
Journal Place: England
Date Published: 2017
Start Page: 1961
End Page: 017-01867-9
Language: eng
DOI/URL:

10.1038/s41467-017-01867-9
Notes: LR: 20171220; JID: 101528555; 2017/03/06 00:00 [received]; 2017/10/20 00:00 [accepted]; 2017/12/08 06:00 [entrez]; 2017/12/08 06:00 [pubmed]; 2017/12/08 06:00 [medline]; epublish