MIF AS A GLUCOCORTICOID-INDUCED MODULATOR OF CYTOKINE PRODUCTION

被引：1002

作者：

CALANDRA, T ^{[1
]}

BERNHAGEN, J ^{[1
]}

METZ, CN ^{[1
]}

SPIEGEL, LA ^{[1
]}

BACHER, M ^{[1
]}

DONNELLY, T ^{[1
]}

CERAMI, A ^{[1
]}

BUCALA, R ^{[1
]}

机构：

[1] PICOWER INST MED RES,MANHASSET,NY 11030

来源：

NATURE | 1995年 / 377卷 / 6544期

关键词：

D O I：

10.1038/377068a0

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

GLUCOCORTICOID hormones are important for vital functions and act to modulate inflammatory and immune responses(1,2). Yet, in contrast to other hormonal systems, no endogenous mediators have been identified that can directly counter-regulate their potent anti-inflammatory and immunosuppressive properties. Recent investigations of the protein macrophage migration inhibitory factor (MIF), which was discovered originally to be a T-lymphocyte-derived factor(3,4), have established it to be a pro-inflammatory pituitary and macrophage cytokine and a critical mediator of septic shock(5-7), Here we report the unexpected finding that low concentrations of glucocorticoids induce rather than inhibit MIF production from macrophages. MIF then acts to override glucocorticoid-mediated inhibition of cytokine secretion by lipopolysaccharide (LPS)-stimulated monocytes acid to overcome glucocorticoid protection against lethal endotoxaemia. These observations identify a unique counter-regulatory system that functions to control inflammatory and immune responses.

引用

页码：68 / 71

页数：4

共 25 条

[1]

ABERNATHY RS, 1957, J LAB CLIN MED, V49, P708

[2]

ARYA SK, 1984, J IMMUNOL, V133, P273

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