CCDC88B is required for pathogenesis of inflammatory bowel disease /631/250/347 /692/699/1503/257/1402 article

Nassima Fodil; Neda Moradin; Vicki Leung; Jean Frederic Olivier; Irena Radovanovic; Thiviya Jeyakumar; Manuel Flores Molina; Ashley McFarquhar; Romain Cayrol; Dominique Bozec; Naglaa H. Shoukry; Michiaki Kubo; Julia Dimitrieva; Edouard Louis; Emilie Theatre; Stephanie Dahan; Yukihide Momozawa; Michel Georges; Garabet Yeretssian; Philippe Gros

doi:10.1038/s41467-017-01381-y

CCDC88B is required for pathogenesis of inflammatory bowel disease /631/250/347 /692/699/1503/257/1402 article

Nassima Fodil, Neda Moradin, Vicki Leung, Jean Frederic Olivier, Irena Radovanovic, Thiviya Jeyakumar, Manuel Flores Molina, Ashley McFarquhar, Romain Cayrol, Dominique Bozec, Naglaa H. Shoukry, Michiaki Kubo, Julia Dimitrieva, Edouard Louis, Emilie Theatre, Stephanie Dahan, Yukihide Momozawa, Michel Georges, Garabet Yeretssian, Philippe Gros

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20 Citations (Scopus)

Abstract

Inflammatory bowel disease (IBD) involves interaction between host genetic factors and environmental triggers. CCDC88B maps within one IBD risk locus on human chromosome 11q13. Here we show that CCDC88B protein increases in the colon during intestinal injury, concomitant with an influx of CCDC88B⁺lymphoid and myeloid cells. Loss of Ccdc88b protects against DSS-induced colitis, with fewer pathological lesions and reduced intestinal inflammation in Ccdc88b-deficient mice. In a T cell transfer model of colitis, Ccdc88b mutant CD4⁺ T cells do not induce colitis in immunocompromised hosts. Expression of human CCDC88B RNA and protein is higher in IBD patient colons than in control colon tissue. In human CD14⁺ myeloid cells, CCDC88B is regulated by cis-acting variants. In a cohort of patients with Crohn's disease, CCDC88B expression correlates positively with disease risk. These findings suggest that CCDC88B has a critical function in colon inflammation and the pathogenesis of IBD.

Original language	English
Article number	932
Journal	Nature communications
Volume	8
Issue number	1
DOIs	https://doi.org/10.1038/s41467-017-01381-y
Publication status	Published - 01-12-2017
Externally published	Yes

All Science Journal Classification (ASJC) codes

General Chemistry
General Biochemistry,Genetics and Molecular Biology
General Physics and Astronomy

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1038/s41467-017-01381-y

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Fodil, N., Moradin, N., Leung, V., Olivier, J. F., Radovanovic, I., Jeyakumar, T., Flores Molina, M., McFarquhar, A., Cayrol, R., Bozec, D., Shoukry, N. H., Kubo, M., Dimitrieva, J., Louis, E., Theatre, E., Dahan, S., Momozawa, Y., Georges, M., Yeretssian, G., & Gros, P. (2017). CCDC88B is required for pathogenesis of inflammatory bowel disease /631/250/347 /692/699/1503/257/1402 article. Nature communications, 8(1), Article 932. https://doi.org/10.1038/s41467-017-01381-y

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title = "CCDC88B is required for pathogenesis of inflammatory bowel disease /631/250/347 /692/699/1503/257/1402 article",

abstract = "Inflammatory bowel disease (IBD) involves interaction between host genetic factors and environmental triggers. CCDC88B maps within one IBD risk locus on human chromosome 11q13. Here we show that CCDC88B protein increases in the colon during intestinal injury, concomitant with an influx of CCDC88B+lymphoid and myeloid cells. Loss of Ccdc88b protects against DSS-induced colitis, with fewer pathological lesions and reduced intestinal inflammation in Ccdc88b-deficient mice. In a T cell transfer model of colitis, Ccdc88b mutant CD4+ T cells do not induce colitis in immunocompromised hosts. Expression of human CCDC88B RNA and protein is higher in IBD patient colons than in control colon tissue. In human CD14+ myeloid cells, CCDC88B is regulated by cis-acting variants. In a cohort of patients with Crohn's disease, CCDC88B expression correlates positively with disease risk. These findings suggest that CCDC88B has a critical function in colon inflammation and the pathogenesis of IBD.",

author = "Nassima Fodil and Neda Moradin and Vicki Leung and Olivier, {Jean Frederic} and Irena Radovanovic and Thiviya Jeyakumar and {Flores Molina}, Manuel and Ashley McFarquhar and Romain Cayrol and Dominique Bozec and Shoukry, {Naglaa H.} and Michiaki Kubo and Julia Dimitrieva and Edouard Louis and Emilie Theatre and Stephanie Dahan and Yukihide Momozawa and Michel Georges and Garabet Yeretssian and Philippe Gros",

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doi = "10.1038/s41467-017-01381-y",

language = "English",

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Fodil, N, Moradin, N, Leung, V, Olivier, JF, Radovanovic, I, Jeyakumar, T, Flores Molina, M, McFarquhar, A, Cayrol, R, Bozec, D, Shoukry, NH, Kubo, M, Dimitrieva, J, Louis, E, Theatre, E, Dahan, S, Momozawa, Y, Georges, M, Yeretssian, G & Gros, P 2017, 'CCDC88B is required for pathogenesis of inflammatory bowel disease /631/250/347 /692/699/1503/257/1402 article', Nature communications, vol. 8, no. 1, 932. https://doi.org/10.1038/s41467-017-01381-y

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T1 - CCDC88B is required for pathogenesis of inflammatory bowel disease /631/250/347 /692/699/1503/257/1402 article

AU - Fodil, Nassima

AU - Moradin, Neda

AU - Leung, Vicki

AU - Olivier, Jean Frederic

AU - Radovanovic, Irena

AU - Jeyakumar, Thiviya

AU - Flores Molina, Manuel

AU - McFarquhar, Ashley

AU - Cayrol, Romain

AU - Bozec, Dominique

AU - Shoukry, Naglaa H.

AU - Kubo, Michiaki

AU - Dimitrieva, Julia

AU - Louis, Edouard

AU - Theatre, Emilie

AU - Dahan, Stephanie

AU - Momozawa, Yukihide

AU - Georges, Michel

AU - Yeretssian, Garabet

AU - Gros, Philippe

PY - 2017/12/1

Y1 - 2017/12/1

N2 - Inflammatory bowel disease (IBD) involves interaction between host genetic factors and environmental triggers. CCDC88B maps within one IBD risk locus on human chromosome 11q13. Here we show that CCDC88B protein increases in the colon during intestinal injury, concomitant with an influx of CCDC88B+lymphoid and myeloid cells. Loss of Ccdc88b protects against DSS-induced colitis, with fewer pathological lesions and reduced intestinal inflammation in Ccdc88b-deficient mice. In a T cell transfer model of colitis, Ccdc88b mutant CD4+ T cells do not induce colitis in immunocompromised hosts. Expression of human CCDC88B RNA and protein is higher in IBD patient colons than in control colon tissue. In human CD14+ myeloid cells, CCDC88B is regulated by cis-acting variants. In a cohort of patients with Crohn's disease, CCDC88B expression correlates positively with disease risk. These findings suggest that CCDC88B has a critical function in colon inflammation and the pathogenesis of IBD.

AB - Inflammatory bowel disease (IBD) involves interaction between host genetic factors and environmental triggers. CCDC88B maps within one IBD risk locus on human chromosome 11q13. Here we show that CCDC88B protein increases in the colon during intestinal injury, concomitant with an influx of CCDC88B+lymphoid and myeloid cells. Loss of Ccdc88b protects against DSS-induced colitis, with fewer pathological lesions and reduced intestinal inflammation in Ccdc88b-deficient mice. In a T cell transfer model of colitis, Ccdc88b mutant CD4+ T cells do not induce colitis in immunocompromised hosts. Expression of human CCDC88B RNA and protein is higher in IBD patient colons than in control colon tissue. In human CD14+ myeloid cells, CCDC88B is regulated by cis-acting variants. In a cohort of patients with Crohn's disease, CCDC88B expression correlates positively with disease risk. These findings suggest that CCDC88B has a critical function in colon inflammation and the pathogenesis of IBD.

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DO - 10.1038/s41467-017-01381-y

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SN - 2041-1723

VL - 8

JO - Nature communications

JF - Nature communications

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ER -

CCDC88B is required for pathogenesis of inflammatory bowel disease /631/250/347 /692/699/1503/257/1402 article

Abstract

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