Development of chronic colitis is dependent on the cytokine MIF

被引：259

作者：

de Jong, YP

Abadia-Molina, AC

Satoskar, AR

Clarke, K

Rietdijk, ST

Faubion, WA

Mizoguchi, E

Metz, CN

Al Sahli, M

ten Hove, T

Keates, AC

Lubetsky, JB

Farrell, RJ

Michetti, P

van Deventer, SJ

Lolis, E

David, JR

Bhan, AK

Terhorst, C ^{[1
]}

机构：

[1] Beth Israel Deaconess Med Ctr, Div Immunol, Boston, MA 02215 USA

[2] Beth Israel Deaconess Med Ctr, Div Gastroenterol, Boston, MA 02215 USA

[3] Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA

[4] Massachusetts Gen Hosp, Immunopathol Unit, Boston, MA 02114 USA

[5] Picower Inst Med Res, Manhasset, NY 11030 USA

[6] Univ Amsterdam, Acad Med Ctr, Expt Med Lab, NL-1105 AZ Amsterdam, Netherlands

[7] Yale Univ, Dept Pharmacol, New Haven, CT 06510 USA

来源：

NATURE IMMUNOLOGY | 2001年 / 2卷 / 11期

关键词：

D O I：

10.1038/ni720

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

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.

引用

收藏

页码：1061 / 1066

页数：6

相关论文

共 32 条

[1] Blockade of interleukin 6 trans signaling suppresses T-cell resistance against apoptosis in chronic intestinal inflammation:: Evidence in Crohn disease and experimental colitis in vivo [J].

Atreya, R ;

Mudter, J ;

Finotto, S ;

Müllberg, J ;

Jostock, T ;

Wirtz, S ;

Schütz, M ;

Bartsch, B ;

Holtmann, M ;

Becker, C ;

Strand, D ;

Czaja, J ;

Schlaak, JF ;

Lehr, HA ;

Autschbach, F ;

Schürmann, G ;

Nishimoto, N ;

Yoshizaki, K ;

Ito, H ;

Kishimoto, T ;

Galle, PR ;

Rose-John, S ;

Neurath, MF .

NATURE MEDICINE, 2000, 6 (05) :583-588

[2] MIF IS A PITUITARY-DERIVED CYTOKINE THAT POTENTIATES LETHAL ENDOTOXEMIA [J].

BERNHAGEN, J ;

CALANDRA, T ;

MITCHELL, RA ;

MARTIN, SB ;

TRACEY, KJ ;

VOELTER, W ;

MANOGUE, KR ;

CERAMI, A ;

BUCALA, R .

NATURE, 1993, 365 (6448) :756-759

[3] MECHANISM OF A REACTION IN VITRO ASSOCIATED WITH DELAYED-TYPE HYPERSENSITIVITY [J].

BLOOM, BR ;

BENNETT, B .

SCIENCE, 1966, 153 (3731) :80-&

[4] Targeted disruption of migration inhibitory factor gene reveals its critical role in sepsis [J].

Bozza, M ;

Satoskar, AR ;

Lin, GS ;

Lu, B ;

Humbles, AA ;

Gerard, C ;

David, JR .

JOURNAL OF EXPERIMENTAL MEDICINE, 1999, 189 (02) :341-346

[5] MACROPHAGE IS AN IMPORTANT AND PREVIOUSLY UNRECOGNIZED SOURCE OF MACROPHAGE-MIGRATION INHIBITORY FACTOR [J].

CALANDRA, T ;

BERNHAGEN, J ;

MITCHELL, RA ;

BUCALA, R .

JOURNAL OF EXPERIMENTAL MEDICINE, 1994, 179 (06) :1895-1902

[6] Macrophage migration inhibitory factor is a critical mediator of the activation of immune cells by exotoxins of gram-positive bacteria [J].

Calandra, T ;

Spiegel, LA ;

Metz, CN ;

Bucala, R .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1998, 95 (19) :11383-11388

[7] Protection from septic shock by neutralization of macrophage migration inhibitory factor [J].

Calandra, T ;

Echtenacher, B ;

Le Roy, D ;

Pugin, J ;

Metz, CN ;

Hültner, L ;

Heumann, D ;

Männel, D ;

Bucala, R ;

Glauser, MP .

NATURE MEDICINE, 2000, 6 (02) :164-170

[8] MIF AS A GLUCOCORTICOID-INDUCED MODULATOR OF CYTOKINE PRODUCTION [J].

CALANDRA, T ;

BERNHAGEN, J ;

METZ, CN ;

SPIEGEL, LA ;

BACHER, M ;

DONNELLY, T ;

CERAMI, A ;

BUCALA, R .

NATURE, 1995, 377 (6544) :68-71

[9] CD4+ T cells reactive to enteric bacterial antigens in spontaneously colitic C3H/HeJBir mice:: Increased T helper cell type 1 response and ability to transfer disease [J].

Cong, YZ ;

Brandwein, SL ;

McCabe, RP ;

Lazenby, A ;

Birkenmeier, EH ;

Sundberg, JP ;

Elson, CO .

JOURNAL OF EXPERIMENTAL MEDICINE, 1998, 187 (06) :855-864

[10] Nonlymphocyte-derived tumor necrosis factor is required for induction of colitis in recombination activating gene (RAG)2-/- mice upon transfer of CD4+CD45RBhi T cells [J].

Corazza, N ;

Eichenberger, S ;

Eugster, HP ;

Mueller, C .

JOURNAL OF EXPERIMENTAL MEDICINE, 1999, 190 (10) :1479-1491

← 1 2 3 4 →