Different Influence of Macrophage Migration Inhibitory Factor (MIF) in Signal Transduction Pathway of Various T Cell Subsets

Immunobiology ◽  
2000 ◽  
Vol 201 (3-4) ◽  
pp. 356-367 ◽  
Author(s):  
Nobuyoshi Kitaichi ◽  
Kazumasa Ogasawara ◽  
Kazuya Iwabuchi ◽  
Jun Nishihira ◽  
Ken-Ichi Namba ◽  
...  
Keyword(s):  
Signal Transduction ◽  
T Cell ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Signal Transduction Pathway ◽  
Inhibitory Factor ◽  
T Cell Subsets ◽  
Macrophage Migration ◽  
Transduction Pathway

Macrophage migration inhibitory factor antagonizes hydrocortisone-induced increases in cytosolic IκBα

2000 ◽  
Vol 279 (3) ◽  
pp. R1043-R1049 ◽  
Author(s):  
Jane M. Daun ◽  
Joseph G. Cannon
Keyword(s):  
Signal Transduction ◽  
Dna Binding ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Inflammatory Cytokine ◽  
Signal Transduction Pathway ◽  
Inhibitory Factor ◽  
Pituitary Cells ◽  
Macrophage Migration ◽  
Transduction Pathway

Macrophage migration inhibitory factor (MIF) is an inflammatory cytokine secreted by several cell types, including mononuclear and pituitary cells. It has also been shown to counteract cortisol-induced inhibition of inflammatory cytokine secretion. The purpose of this study was to determine whether MIF antagonized the effect of hydrocortisone on the NF-κB/IκB signal transduction pathway in lipopolysaccharide (LPS)-stimulated human peripheral blood mononuclear cells. Physiological doses of hydrocortisone (50–200 ng/ml) diminished both the LPS-stimulated decrease in cytosolic IκBα levels and the subsequent increase in nuclear NF-κB DNA binding. In the presence of both LPS and hydrocortisone, 1 ng/ml of MIF antagonized the effects of hydrocortisone, resulting in decreased cytosolic IκBα levels ( P < 0.05) and increased nuclear NF-κB DNA binding ( P < 0.05). In the absence of hydrocortisone, MIF had no effect on LPS-induced decreases in IκBα. In the absence of LPS, MIF inhibited hydrocortisone-induced increases in IκBα ( P = 0.03). Thus the mechanism by which MIF antagonizes the effect of hydrocortisone on the NF-kB/IκB signal transduction pathway is through inhibiting the ability of hydrocortisone to increase cytosolic IκBα.

scholarly journals Role of Macrophage Migration Inhibitory Factor in the Regulatory T Cell Response of Tumor-Bearing Mice

2012 ◽  
Vol 189 (8) ◽  
pp. 3905-3913 ◽  
Author(s):  
Susanna Choi ◽  
Hang-Rae Kim ◽  
Lin Leng ◽  
Insoo Kang ◽  
William L. Jorgensen ◽  
...  
Keyword(s):  
T Cell ◽  
Migration Inhibitory Factor ◽  
Regulatory T Cell ◽  
Cell Response ◽  
Macrophage Migration Inhibitory Factor ◽  
T Cell Response ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Tumor Bearing

scholarly journals An integrated signal transduction network of macrophage migration inhibitory factor

2016 ◽  
Vol 10 (2) ◽  
pp. 165-170 ◽  
Author(s):  
Tejaswini Subbannayya ◽  
Prathyaksha Variar ◽  
Jayshree Advani ◽  
Bipin Nair ◽  
Subramanian Shankar ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Signal Transduction Network

scholarly journals Glioblastoma myeloid-derived suppressor cell subsets express differential macrophage migration inhibitory factor receptor profiles that can be targeted to reduce immune suppression

2019 ◽  
Author(s):  
Tyler J. Alban ◽  
Defne Bayik ◽  
Balint Otvos ◽  
Anja Rabljenovic ◽  
Lin Leng ◽  
...  
Keyword(s):  
T Cell ◽  
Tumor Microenvironment ◽  
Immune Suppression ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Cell Activity ◽  
Suppressor Cell ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Cognate Receptor

AbstractThe application of tumor immunotherapy to glioblastoma (GBM) is limited by an unprecedented degree of immune suppression due to factors that include high numbers of immune suppressive myeloid cells, the blood brain barrier, and T cell sequestration to the bone marrow. We previously identified an increase in immune suppressive myeloid-derived suppressor cells (MDSCs) in GBM patients, which correlated with poor prognosis and was dependent on macrophage migration inhibitory factor (MIF). Here we examine the MIF signaling axis in detail in murine MDSC models, GBM-educated MDSCs and human GBM. We found that the monocytic subset of MDSCs (M-MDSCs), expressed high levels of the MIF cognate receptor CD74 and was localized in the tumor microenvironment. In contrast, granulocytic MDSCs (G-MDSCs) expressed high levels of the MIF non-cognate receptor CXCR2 and showed minimal accumulation in the tumor microenvironment. Furthermore, targeting M-MDSCs with ibudilast, a brain penetrant MIF-CD74 interaction inhibitor, reduced MDSC function and enhanced CD8 T cell activity in the tumor microenvironment. These findings demonstrate the MDSC subsets differentially express MIF receptors and may be leveraged for specific MDSC targeting.

scholarly journals Macrophage Migration Inhibitory Factor: A Downregulator of Early T Cell-Dependent IFN-γ Responses inPlasmodium chabaudi adami(556 KA)-Infected Mice

2011 ◽  
Vol 186 (11) ◽  
pp. 6271-6279 ◽  
Author(s):  
Diane Tshikudi Malu ◽  
Benoit Bélanger ◽  
François Desautels ◽  
Karine Kelendji ◽  
Esther Dalko ◽  
...  
Keyword(s):  
T Cell ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Ifn Γ
Sign in / Sign up

Export Citation Format

Share Document