title: Potentiation of Th17 cytokines in aging process contributes to the development of colitis.
abstract: Th17 cells, which produce IL-17 and IL-22, promote autoimmunity in mice and have been implicated in the pathogenesis of autoimmune/inflammatory diseases in humans. However, the Th17 immune response in the aging process is still not clear. In the present study, we found that the induction of IL-17-producing CD4(+) T cells was significantly increased in aged individuals compared with young healthy ones. The mRNA expression of IL-17, IL-17F, IL-22, and RORC2 was also significantly increased in aged people. Similar to humans, Th17 cells as well as mRNAs encoding IL-17, IL-22 and RORγt were dramatically elevated in naïve T cells from aged mouse compared to young ones. In addition, CD44 positive IL-17-producing CD4(+) T cells were significantly higher in aged mice, suggesting that memory T cells are an important source of IL-17 production. Furthermore, the percentage of IL-17-producing CD4(+) T cells generated in co-culture with dendritic cells from either aged or young mice did not show significant differences, suggesting that dendritic cells do not play a primary role in the elevation of Th17 cytokines in aged mouse cells. Importantly, transfer of CD4(+)CD45Rb(hi) cells from aged mice induced more severe colitis in RAG(-/-) mice compared to cells from young mice, Taken together, these results suggest that Th17 immune responses are elevated in aging humans and mice and may contribute to the increased development of inflammatory disorders in the elderly.
authors.affiliation: Immunology Institute, Mount Sinai School of Medicine, New York, NY 10029, United States.
authors.forename: Xinshou
authors.initials: X
authors.lastname: Ouyang
authors.forename: Zhuoshun
authors.initials: Z
authors.lastname: Yang
authors.forename: Ruihua
authors.initials: R
authors.lastname: Zhang
authors.forename: Paul
authors.initials: P
authors.lastname: Arnaboldi
authors.forename: Geming
authors.initials: G
authors.lastname: Lu
authors.forename: Qingshan
authors.initials: Q
authors.lastname: Li
authors.forename: Weidong
authors.initials: W
authors.lastname: Wang
authors.forename: Biao
authors.initials: B
authors.lastname: Zhang
authors.forename: Miao
authors.initials: M
authors.lastname: Cui
authors.forename: Huafeng
authors.initials: H
authors.lastname: Zhang
authors.forename: Jane
authors.initials: J
authors.lastname: Liang-Chen
authors.forename: Lihui
authors.initials: L
authors.lastname: Qin
authors.forename: Feng
authors.initials: F
authors.lastname: Zheng
authors.forename: Bo
authors.initials: B
authors.lastname: Huang
authors.forename: Huabao
authors.initials: H
authors.lastname: Xiong
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000375:Aging / Q000276:immunology*; D000818:Animals; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D018920:Coculture Techniques; D003092:Colitis / Q000276:immunology*; D016207:Cytokines / Q000276:immunology*; D003713:Dendritic Cells / Q000276:immunology; D005260:Female; D006801:Humans; D018960:Hyaluronan Receptors / Q000276:immunology; D020381:Interleukin-17 / Q000276:immunology; D007378:Interleukins / Q000276:immunology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3 / Q000276:immunology; D058504:Th17 Cells / Q000276:immunology*; D055815:Young Adult; D000097043:Interleukin-22
chemical_list: D016207:Cytokines; D018960:Hyaluronan Receptors; D020381:Interleukin-17; D007378:Interleukins; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3; D000097043:Interleukin-22; C476399:Cd44 protein, mouse