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Redundant Innate and Adaptive Sources of IL17 Production Drive Colon Tumorigenesis
Cancer research (Chicago, Ill.), 2016-04, Vol.76 (8), p.2115-2124
Housseau, Franck
Wu, Shaoguang
Wick, Elizabeth C
Fan, Hongni
Wu, Xinqun
Llosa, Nicolas J
Smith, Kellie N
Tam, Ada
Ganguly, Sudipto
Wanyiri, Jane W
Iyadorai, Thevambiga
Malik, Ausama A
Roslani, April C
Vadivelu, Jamunarani S
Van Meerbeke, Sara
Huso, David L
Pardoll, Drew M
Sears, Cynthia L
2016
Details
Autor(en) / Beteiligte
Housseau, Franck
Wu, Shaoguang
Wick, Elizabeth C
Fan, Hongni
Wu, Xinqun
Llosa, Nicolas J
Smith, Kellie N
Tam, Ada
Ganguly, Sudipto
Wanyiri, Jane W
Iyadorai, Thevambiga
Malik, Ausama A
Roslani, April C
Vadivelu, Jamunarani S
Van Meerbeke, Sara
Huso, David L
Pardoll, Drew M
Sears, Cynthia L
Titel
Redundant Innate and Adaptive Sources of IL17 Production Drive Colon Tumorigenesis
Ist Teil von
Cancer research (Chicago, Ill.), 2016-04, Vol.76 (8), p.2115-2124
Ort / Verlag
United States
Erscheinungsjahr
2016
Link zum Volltext
Quelle
MEDLINE
Beschreibungen/Notizen
IL17-producing Th17 cells, generated through a STAT3-dependent mechanism, have been shown to promote carcinogenesis in many systems, including microbe-driven colon cancer. Additional sources of IL17, such as γδ T cells, become available under inflammatory conditions, but their contributions to cancer development are unclear. In this study, we modeled Th17-driven colon tumorigenesis by colonizing Min(Ap) (c+/-) mice with the human gut bacterium, enterotoxigenic Bacteroides fragilis (ETBF), to investigate the link between inflammation and colorectal cancer. We found that ablating Th17 cells by knocking out Stat3 in CD4(+) T cells delayed tumorigenesis, but failed to suppress the eventual formation of colonic tumors. However, IL17 blockade significantly attenuated tumor formation, indicating a critical requirement for IL17 in tumorigenesis, but from a source other than Th17 cells. Notably, genetic ablation of γδ T cells in ETBF-colonized Th17-deficient Min mice prevented the late emergence of colonic tumors. Taken together, these findings support a redundant role for adaptive Th17 cell- and innate γδT17 cell-derived IL17 in bacteria-induced colon carcinogenesis, stressing the importance of therapeutically targeting the cytokine itself rather than its cellular sources. Cancer Res; 76(8); 2115-24. ©2016 AACR.
Sprache
Englisch
Identifikatoren
ISSN: 0008-5472
eISSN: 1538-7445
DOI: 10.1158/0008-5472.can-15-0749
Titel-ID: cdi_proquest_miscellaneous_1790462412
Format
–
Schlagworte
Adaptive Immunity
,
Animals
,
Carcinogenesis
,
CD4 Antigens - immunology
,
Colonic Neoplasms - immunology
,
Colonic Neoplasms - metabolism
,
Colonic Neoplasms - pathology
,
Humans
,
Immunity, Innate
,
Interleukin-17 - biosynthesis
,
Mice
,
Mice, Inbred C57BL
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