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A pathogenic role for T cell-derived IL-22BP in inflammatory bowel disease

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A pathogenic role for T cell-derived IL-22BP in inflammatory bowel disease. / Pelczar, Penelope; Witkowski, Mario; Perez, Laura Garcia; Kempski, Jan; Hammel, Anna G; Brockmann, Leonie; Kleinschmidt, Dörte; Wende, Sandra; Haueis, Cathleen; Bedke, Tanja; Krasemann, Susanne; Steurer, Stefan; Booth, Carmen J; Busch, Christoph Philipp; König, Alexandra; Rauch, Ursula; Benten, Daniel; Izbicki, Jakob R; Rösch, Thomas; Lohse, Ansgar W; Strowig, Till; Gagliani, Nicola; Flavell, Richard A; Huber, Samuel.

in: SCIENCE, Jahrgang 354, Nr. 6310, 21.10.2016, S. 358-362.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Pelczar, P, Witkowski, M, Perez, LG, Kempski, J, Hammel, AG, Brockmann, L, Kleinschmidt, D, Wende, S, Haueis, C, Bedke, T, Krasemann, S, Steurer, S, Booth, CJ, Busch, CP, König, A, Rauch, U, Benten, D, Izbicki, JR, Rösch, T, Lohse, AW, Strowig, T, Gagliani, N, Flavell, RA & Huber, S 2016, 'A pathogenic role for T cell-derived IL-22BP in inflammatory bowel disease', SCIENCE, Jg. 354, Nr. 6310, S. 358-362. https://doi.org/10.1126/science.aah5903

APA

Pelczar, P., Witkowski, M., Perez, L. G., Kempski, J., Hammel, A. G., Brockmann, L., Kleinschmidt, D., Wende, S., Haueis, C., Bedke, T., Krasemann, S., Steurer, S., Booth, C. J., Busch, C. P., König, A., Rauch, U., Benten, D., Izbicki, J. R., Rösch, T., ... Huber, S. (2016). A pathogenic role for T cell-derived IL-22BP in inflammatory bowel disease. SCIENCE, 354(6310), 358-362. https://doi.org/10.1126/science.aah5903

Vancouver

Pelczar P, Witkowski M, Perez LG, Kempski J, Hammel AG, Brockmann L et al. A pathogenic role for T cell-derived IL-22BP in inflammatory bowel disease. SCIENCE. 2016 Okt 21;354(6310):358-362. https://doi.org/10.1126/science.aah5903

Bibtex

@article{69256d345e37421e86b8168dd45e84f5,
title = "A pathogenic role for T cell-derived IL-22BP in inflammatory bowel disease",
abstract = "Intestinal inflammation can impair mucosal healing, thereby establishing a vicious cycle leading to chronic inflammatory bowel disease (IBD). However, the signaling networks driving chronic inflammation remain unclear. Here we report that CD4(+) T cells isolated from patients with IBD produce high levels of interleukin-22 binding protein (IL-22BP), the endogenous inhibitor of the tissue-protective cytokine IL-22. Using mouse models, we demonstrate that IBD development requires T cell-derived IL-22BP. Lastly, intestinal CD4(+) T cells isolated from IBD patients responsive to treatment with antibodies against tumor necrosis factor-α (anti-TNF-α), the most effective known IBD therapy, exhibited reduced amounts of IL-22BP expression but still expressed IL-22. Our findings suggest that anti-TNF-α therapy may act at least in part by suppressing IL-22BP and point toward a more specific potential therapy for IBD.POM-Newsletter",
author = "Penelope Pelczar and Mario Witkowski and Perez, {Laura Garcia} and Jan Kempski and Hammel, {Anna G} and Leonie Brockmann and D{\"o}rte Kleinschmidt and Sandra Wende and Cathleen Haueis and Tanja Bedke and Susanne Krasemann and Stefan Steurer and Booth, {Carmen J} and Busch, {Christoph Philipp} and Alexandra K{\"o}nig and Ursula Rauch and Daniel Benten and Izbicki, {Jakob R} and Thomas R{\"o}sch and Lohse, {Ansgar W} and Till Strowig and Nicola Gagliani and Flavell, {Richard A} and Samuel Huber",
note = "Copyright {\textcopyright} 2016, American Association for the Advancement of Science.",
year = "2016",
month = oct,
day = "21",
doi = "10.1126/science.aah5903",
language = "English",
volume = "354",
pages = "358--362",
journal = "SCIENCE",
issn = "0036-8075",
publisher = "American Association for the Advancement of Science",
number = "6310",

}

RIS

TY - JOUR

T1 - A pathogenic role for T cell-derived IL-22BP in inflammatory bowel disease

AU - Pelczar, Penelope

AU - Witkowski, Mario

AU - Perez, Laura Garcia

AU - Kempski, Jan

AU - Hammel, Anna G

AU - Brockmann, Leonie

AU - Kleinschmidt, Dörte

AU - Wende, Sandra

AU - Haueis, Cathleen

AU - Bedke, Tanja

AU - Krasemann, Susanne

AU - Steurer, Stefan

AU - Booth, Carmen J

AU - Busch, Christoph Philipp

AU - König, Alexandra

AU - Rauch, Ursula

AU - Benten, Daniel

AU - Izbicki, Jakob R

AU - Rösch, Thomas

AU - Lohse, Ansgar W

AU - Strowig, Till

AU - Gagliani, Nicola

AU - Flavell, Richard A

AU - Huber, Samuel

N1 - Copyright © 2016, American Association for the Advancement of Science.

PY - 2016/10/21

Y1 - 2016/10/21

N2 - Intestinal inflammation can impair mucosal healing, thereby establishing a vicious cycle leading to chronic inflammatory bowel disease (IBD). However, the signaling networks driving chronic inflammation remain unclear. Here we report that CD4(+) T cells isolated from patients with IBD produce high levels of interleukin-22 binding protein (IL-22BP), the endogenous inhibitor of the tissue-protective cytokine IL-22. Using mouse models, we demonstrate that IBD development requires T cell-derived IL-22BP. Lastly, intestinal CD4(+) T cells isolated from IBD patients responsive to treatment with antibodies against tumor necrosis factor-α (anti-TNF-α), the most effective known IBD therapy, exhibited reduced amounts of IL-22BP expression but still expressed IL-22. Our findings suggest that anti-TNF-α therapy may act at least in part by suppressing IL-22BP and point toward a more specific potential therapy for IBD.POM-Newsletter

AB - Intestinal inflammation can impair mucosal healing, thereby establishing a vicious cycle leading to chronic inflammatory bowel disease (IBD). However, the signaling networks driving chronic inflammation remain unclear. Here we report that CD4(+) T cells isolated from patients with IBD produce high levels of interleukin-22 binding protein (IL-22BP), the endogenous inhibitor of the tissue-protective cytokine IL-22. Using mouse models, we demonstrate that IBD development requires T cell-derived IL-22BP. Lastly, intestinal CD4(+) T cells isolated from IBD patients responsive to treatment with antibodies against tumor necrosis factor-α (anti-TNF-α), the most effective known IBD therapy, exhibited reduced amounts of IL-22BP expression but still expressed IL-22. Our findings suggest that anti-TNF-α therapy may act at least in part by suppressing IL-22BP and point toward a more specific potential therapy for IBD.POM-Newsletter

U2 - 10.1126/science.aah5903

DO - 10.1126/science.aah5903

M3 - SCORING: Journal article

C2 - 27846573

VL - 354

SP - 358

EP - 362

JO - SCIENCE

JF - SCIENCE

SN - 0036-8075

IS - 6310

ER -