Macrophage migration inhibitory factor: a regulator of innate immunity

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I-43: Expression Profile of Macrophage Migration Inhibitory Factor (MIF) Signaling Pathway as A Potentional Biomarker in Pathophysiology of Endometriosis

Background MIF via its receptor, CD74, initiates a signaling cascade that leads to proliferation and survival of cells. Also, MIF binding to CD74 activates p38 signaling pathways that lead to positive effect on the expression of COX-2. The aim of this study was to evaluate the gene expression profile of MIF, CD74 and COX-2 in normal, ectopic and eutopic endometrium during menstrual cycle. The e...

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Glucocorticoid Suppression of Macrophage Migration Inhibitory Factor

The ability of hydrocortisone to modify antigen-mediated inhibition of macrophage migration, an in vitro correlate of cellular immunity in the guinea pig, was investigated. Only the glucocorticoids, hydrocortisone and dexamethasone, significantly blocked migration inhibitory factor (MIF) activity in pharmacologic concentrations. Hydrocortisone had no effect on antigen "processing" by macrophage...

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Correlation between urine macrophage migration inhibitory factor (MIF)/creatinine ratio and time after kidney transplantation

 Abstract  Background: Despite the long-standing association of macrophage migration inhibitory  factor (MIF) with delayed-type hypersensitivity response, the potential role  of MIF in chronic allograft nephropathy is unknown. The association between upregulation of MIF expression, macrophage and T cell infiltration and the severity of  chronic allograft nephropathy suggests that MIF may be an ...

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Macrophage Migration Inhibitory Factor in Protozoan Infections

Macrophage migration inhibitory factor (MIF) is a cytokine that plays a central role in immune and inflammatory responses. In the present paper, we discussed the participation of MIF in the immune response to protozoan parasite infections. As a general trend, MIF participates in the control of parasite burden at the expense of promoting tissue damage due to increased inflammation.

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ژورنال

عنوان ژورنال: Nature Reviews Immunology

سال: 2003

ISSN: 1474-1733,1474-1741

DOI: 10.1038/nri1200