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

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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

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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

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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.).",

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doi = "10.1038/ni720",

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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

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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.

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Development of chronic colitis is dependent on the cytokine MIF

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