Development of chronic colitis is dependent on the cytokine MIF

Ype P. De Jong; Ana C. Abadia-Molina; Abhay R. Satoskar; Kareem Clarke; Svend T. Rietdijk; William A. Faubion; Emiko Mizoguchi; Christine N. Metz; Mazen Al Sahli; Tessa Ten Hove; Andrew C. Keates; Jodi B. Lubetsky; Richard J. Farrell; Pierre Michetti; Sander J. Van Deventer; Elias Lolis; John R. David; Atul K. Bhan; Cox Terhorst

doi:10.1038/ni720

Development of chronic colitis is dependent on the cytokine MIF

Ype P. De Jong, Ana C. Abadia-Molina, Abhay R. Satoskar, Kareem Clarke, Svend T. Rietdijk, William A. Faubion, Emiko Mizoguchi, Christine N. Metz, Mazen Al Sahli, Tessa Ten Hove, Andrew C. Keates, Jodi B. Lubetsky, Richard J. Farrell, Pierre Michetti, Sander J. Van Deventer, Elias Lolis, John R. David, Atul K. Bhan, Cox Terhorst

Research output: Contribution to journal › Article › peer-review

265 Scopus citations

Abstract

The cytokine macrophage-migration inhibitory factor (MIF) is secreted by a number of cell types upon induction by lipopolysaccharide (LPS). Because colitis is dependent on interplay between the mucosal immune system and intestinal bacteria, we investigated the role of MIF in experimental colitis. MIF-deficient mice failed to develop disease, but reconstitution of MIF-deficient mice with wild-type innate immune cells restored colitis. In addition, established colitis could be treated with anti-MIF immunoglobulins. Thus, murine colitis is dependent on continuous MIF production by the innate immune system. Because we found increased plasma MIF concentrations in patients with Crohn's disease, these data suggested that MIF is a new target for intervention in Crohn's disease.

Original language	English (US)
Pages (from-to)	1061-1066
Number of pages	6
Journal	Nature immunology
Volume	2
Issue number	11
DOIs	https://doi.org/10.1038/ni720
State	Published - 2001

ASJC Scopus subject areas

Immunology and Allergy
Immunology

Access to Document

10.1038/ni720

Cite this

De Jong, Y. P., Abadia-Molina, A. C., Satoskar, A. R., Clarke, K., Rietdijk, S. T., Faubion, W. A., Mizoguchi, E., Metz, C. N., Sahli, M. A., Ten Hove, T., Keates, A. C., Lubetsky, J. B., Farrell, R. J., Michetti, P., Van Deventer, S. J., Lolis, E., David, J. R., Bhan, A. K., & Terhorst, C. (2001). Development of chronic colitis is dependent on the cytokine MIF. Nature immunology, 2(11), 1061-1066. https://doi.org/10.1038/ni720

De Jong, YP, Abadia-Molina, AC, Satoskar, AR, Clarke, K, Rietdijk, ST, Faubion, WA, Mizoguchi, E, Metz, CN, Sahli, MA, Ten Hove, T, Keates, AC, Lubetsky, JB, Farrell, RJ, Michetti, P, Van Deventer, SJ, Lolis, E, David, JR, Bhan, AK & Terhorst, C 2001, 'Development of chronic colitis is dependent on the cytokine MIF', Nature immunology, vol. 2, no. 11, pp. 1061-1066. https://doi.org/10.1038/ni720

@article{0192dd0544f244fcae55ee1fe30af0a2,

title = "Development of chronic colitis is dependent on the cytokine MIF",

abstract = "The cytokine macrophage-migration inhibitory factor (MIF) is secreted by a number of cell types upon induction by lipopolysaccharide (LPS). Because colitis is dependent on interplay between the mucosal immune system and intestinal bacteria, we investigated the role of MIF in experimental colitis. MIF-deficient mice failed to develop disease, but reconstitution of MIF-deficient mice with wild-type innate immune cells restored colitis. In addition, established colitis could be treated with anti-MIF immunoglobulins. Thus, murine colitis is dependent on continuous MIF production by the innate immune system. Because we found increased plasma MIF concentrations in patients with Crohn's disease, these data suggested that MIF is a new target for intervention in Crohn's disease.",

author = "{De Jong}, {Ype P.} and Abadia-Molina, {Ana C.} and Satoskar, {Abhay R.} and Kareem Clarke and Rietdijk, {Svend T.} and Faubion, {William A.} and Emiko Mizoguchi and Metz, {Christine N.} and Sahli, {Mazen Al} and {Ten Hove}, Tessa and Keates, {Andrew C.} and Lubetsky, {Jodi B.} and Farrell, {Richard J.} and Pierre Michetti and {Van Deventer}, {Sander J.} and Elias Lolis and David, {John R.} and Bhan, {Atul K.} and Cox Terhorst",

note = "Funding Information: Acknowledgments We thank D. Podolsky for critically reviewing the manuscript,A. Meinhardt for technical advice and G. Lin for assistance with genotyping mice. Supported by grants from the National Institutes of Health (DK52510 to C.T.; DK47677 to A. K. B.;AI25532 to J. R. D.; DK43351 to C.T. and A. K. B.) and the Crohn{\textquoteright}s and Colitis Foundation of America (Y. P. J.).",

year = "2001",

doi = "10.1038/ni720",

language = "English (US)",

volume = "2",

pages = "1061--1066",

journal = "Nature immunology",

issn = "1529-2908",

publisher = "Nature Publishing Group",

number = "11",

}

TY - JOUR

T1 - Development of chronic colitis is dependent on the cytokine MIF

AU - De Jong, Ype P.

AU - Abadia-Molina, Ana C.

AU - Satoskar, Abhay R.

AU - Clarke, Kareem

AU - Rietdijk, Svend T.

AU - Faubion, William A.

AU - Mizoguchi, Emiko

AU - Metz, Christine N.

AU - Sahli, Mazen Al

AU - Ten Hove, Tessa

AU - Keates, Andrew C.

AU - Lubetsky, Jodi B.

AU - Farrell, Richard J.

AU - Michetti, Pierre

AU - Van Deventer, Sander J.

AU - Lolis, Elias

AU - David, John R.

AU - Bhan, Atul K.

AU - Terhorst, Cox

N1 - Funding Information: Acknowledgments We thank D. Podolsky for critically reviewing the manuscript,A. Meinhardt for technical advice and G. Lin for assistance with genotyping mice. Supported by grants from the National Institutes of Health (DK52510 to C.T.; DK47677 to A. K. B.;AI25532 to J. R. D.; DK43351 to C.T. and A. K. B.) and the Crohn’s and Colitis Foundation of America (Y. P. J.).

PY - 2001

Y1 - 2001

N2 - The cytokine macrophage-migration inhibitory factor (MIF) is secreted by a number of cell types upon induction by lipopolysaccharide (LPS). Because colitis is dependent on interplay between the mucosal immune system and intestinal bacteria, we investigated the role of MIF in experimental colitis. MIF-deficient mice failed to develop disease, but reconstitution of MIF-deficient mice with wild-type innate immune cells restored colitis. In addition, established colitis could be treated with anti-MIF immunoglobulins. Thus, murine colitis is dependent on continuous MIF production by the innate immune system. Because we found increased plasma MIF concentrations in patients with Crohn's disease, these data suggested that MIF is a new target for intervention in Crohn's disease.

AB - The cytokine macrophage-migration inhibitory factor (MIF) is secreted by a number of cell types upon induction by lipopolysaccharide (LPS). Because colitis is dependent on interplay between the mucosal immune system and intestinal bacteria, we investigated the role of MIF in experimental colitis. MIF-deficient mice failed to develop disease, but reconstitution of MIF-deficient mice with wild-type innate immune cells restored colitis. In addition, established colitis could be treated with anti-MIF immunoglobulins. Thus, murine colitis is dependent on continuous MIF production by the innate immune system. Because we found increased plasma MIF concentrations in patients with Crohn's disease, these data suggested that MIF is a new target for intervention in Crohn's disease.

UR - http://www.scopus.com/inward/record.url?scp=17944369782&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=17944369782&partnerID=8YFLogxK

U2 - 10.1038/ni720

DO - 10.1038/ni720

M3 - Article

C2 - 11668338

AN - SCOPUS:17944369782

SN - 1529-2908

VL - 2

SP - 1061

EP - 1066

JO - Nature immunology

JF - Nature immunology

IS - 11

ER -

Development of chronic colitis is dependent on the cytokine MIF

Abstract

ASJC Scopus subject areas

Access to Document

Other files and links

Fingerprint

Cite this