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

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 Usefulness of the IgA and IgG Responses to Macrophage Migration Inhibitory Factor for the Diagnosis of Tuberculosis

Diagnostics ◽  
2020 ◽  
Vol 10 (11) ◽  
pp. 991
Author(s):  
Ji Yeon Lee ◽  
Byoung-Jun Kim ◽  
Jee-min Kim ◽  
Junghyun Kim ◽  
Joon-Sung Joh ◽  
...  
Keyword(s):  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Latent Tuberculosis ◽  
Protective Role ◽  
Antibody Responses ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Serological Tests ◽  
Iga Antibody ◽  
Ifn Γ

Serological tests offer the potential in order to improve the diagnosis of tuberculosis (TB). Macrophage migration inhibitory factor (MIF) plays a protective role in infection control in TB; however, to date, no studies on antibody responses to MIF have been reported. We measured immunoglobulin (Ig)A and IgG responses to MIF in individuals with either active tuberculosis (ATB; n = 65), latent tuberculosis (LTBI; n = 53), or in non-infected individuals (NI; n = 62). The QuantiFERON-TB Gold In-Tube (QFT-GIT) assay was used in order to screen for LTBI. The level of IgA against MIF was significantly lower in LTBI and ATB patients than in NI individuals, was significantly related to LTBI and ATB diagnosis, and it could discriminate between LTBI and ATB. In contrast, the level of IgG against MIF was significantly lower in LTBI patients than in NI individuals and was significantly related to LTBI diagnosis. Anti-MIF IgG levels were significantly lower in AFB-negative TB, minimal TB, and new ATB patients, than in the NI group. IgA and IgG levels against MIF both showed significant negative correlations with IFN-γ levels, as assessed using the QFT-GIT test. Although none of the antibodies could achieve high diagnostic predictive power individually, our results suggest the possibility of using IgA antibody responses to MIF in the diagnosis of LTBI and ATB.

scholarly journals Macrophage Migration Inhibitory Factor Contributes to Host Defense against Acute Trypanosoma cruzi Infection

2006 ◽  
Vol 74 (6) ◽  
pp. 3170-3179 ◽  
Author(s):  
José L. Reyes ◽  
Luis I. Terrazas ◽  
Bertha Espinoza ◽  
David Cruz-Robles ◽  
Virgilia Soto ◽  
...  
Keyword(s):  
Trypanosoma Cruzi ◽  
Host Defense ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Inhibitory Factor ◽  
Interleukin 12 ◽  
Macrophage Migration ◽  
Necrosis Factor Alpha ◽  
Ifn Γ ◽  
Oxide Synthase

ABSTRACT Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine that is involved in the host defense against several pathogens. Here we used MIF−/− mice to determine the role of endogenous MIF in the regulation of the host immune response against Trypanosoma cruzi infection. MIF−/− mice displayed high levels of blood and tissue parasitemia, developed severe heart and skeletal muscle immunopathology, and succumbed to T. cruzi infection faster than MIF+/+ mice. The enhanced susceptibility of MIF−/− mice to T. cruzi was associated with reduced levels of proinflammatory cytokines, such as tumor necrosis factor alpha, interleukin-12 (IL-12), IL-18, gamma interferon (IFN-γ), and IL-1β, in their sera and reduced production of IL-12, IFN-γ, and IL-4 by spleen cells during the early phase of infection. At all time points, antigen-stimulated splenocytes from MIF+/+ and MIF−/− mice produced comparable levels of IL-10. MIF−/− mice also produced significantly less Th1-associated antigen-specific immunoglobulin G2a (IgG2a) throughout the infection, but both groups produced comparable levels of Th2-associated IgG1. Lastly, inflamed hearts from T. cruzi-infected MIF−/− mice expressed increased transcripts for IFN-γ, but fewer for IL-12 p35, IL-12 p40, IL-23, and inducible nitric oxide synthase, compared to MIF+/+ mice. Taken together, our findings show that MIF plays a role in controlling acute T. cruzi infection.

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.

Sign in / Sign up

Export Citation Format

Share Document