scholarly journals IL-21–Induced MHC Class II+ NK Cells Promote the Expansion of Human Uncommitted CD4+ Central Memory T Cells in a Macrophage Migration Inhibitory Factor–Dependent Manner

2016 ◽  
Vol 197 (1) ◽  
pp. 85-96 ◽  
Author(s):  
Romain Loyon ◽  
Emilie Picard ◽  
Olivier Mauvais ◽  
Lise Queiroz ◽  
Virginie Mougey ◽  
...  
Keyword(s):  
T Cells ◽  
Nk Cells ◽  
Mhc Class Ii ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Memory T Cells ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Dependent Manner ◽  
Central Memory T Cells

scholarly journals Human decidual natural killer cells as a source and target of macrophage migration inhibitory factor

Reproduction ◽  
2006 ◽  
Vol 131 (1) ◽  
pp. 175-182 ◽  
Author(s):  
F Arcuri ◽  
M Cintorino ◽  
A Carducci ◽  
S Papa ◽  
M G Riparbelli ◽  
...  
Keyword(s):  
Nk Cells ◽  
Natural Killer ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
K562 Cells ◽  
Cytolytic Activity ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Dependent Manner ◽  
Unk Cells

The human uterine mucosa of early pregnancy is largely populated by CD56brightnatural killer (NK) cells (uterine (u) NK cells). The specific functions of these cells are still unknown, but their interaction and response to foetal trophoblasts are thought to be important for the establishment of a successful pregnancy. The study reported herein shows that uNK cells respond to, and produce, macrophage migration inhibitory factor (MIF), a cytokine highly expressed in the human placenta and in the cyclic and pregnant endometrium. Recombinant human MIF reduced in a dose-dependent manner the cytolytic activity of purified uNK cells against K562 cells. RT-PCR, Western blot analysis and ELISA demonstrated the synthesis and secretion of the cytokine by uNK cells. Double immunofluorescence staining showed the presence of MIF in uterine CD56 + cells. Finally, neutralization of the endogenous cytokine by a polyclonal antibody resulted in a sharp increase in the cytolytic activity of uNK cells. These findings indicate the existence of a previously unrevealed paracrine and autocrine action of MIF on uNK cells and support its contribution to the immune privilege at the maternal–foetal interface.

scholarly journals Overexpression of Macrophage Migration Inhibitory Factor and Its Homologue D-Dopachrome Tautomerase as Negative Prognostic Factor in Neuroblastoma

2019 ◽  
Vol 9 (10) ◽  
pp. 284 ◽  
Author(s):  
Eugenio Cavalli ◽  
Emanuela Mazzon ◽  
Santa Mammana ◽  
Maria Basile ◽  
Salvo Lombardo ◽  
...  
Keyword(s):  
T Cells ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Cytotoxic T Cells ◽  
Hdac Inhibitors ◽  
Inhibitory Factor ◽  
Mycn Amplification ◽  
Macrophage Migration ◽  
Dopachrome Tautomerase

Neuroblastoma (NB) represents one of the most frequent pediatric solid tumors. Macrophage migration inhibitory factor (MIF) is a cytokine exerting multiple biological functions. More recently, a second member of the MIF family of cytokine has been identified, the D-dopachrome tautomerase (DDT), that exerts several overlapping functions with MIF. Growing evidence suggests a key role for MIF and DDT in the development of cancer. The aim of this study is to characterize the prognostic value of MIF and DDT in NB. We show that higher expression levels of MIF and DDT in Stage 4 NB samples are associated with a poorer prognosis, independently of the presence of MYCN amplification. Moreover, higher levels of MIF are mostly enriched by Th1 cells, while lower levels of MIF are associated with an increased proportion of B cells, Cytotoxic T cells, Dendritic cells and Natural Killer T cells. We also show that treatment with the histone deacetylase (HDAC) inhibitor, vorinostat, of the NB cell line, SH-SY5Y, determines a significant reduction in the expression of both MIF and DDT. Finally, MIF and DDT inhibition by short interfering RNA is able to revert vincristine sensitivity in vitro. Overall, our data suggest that MIF exert pro-tumorigenic properties in NB, likely by dampening antigen presentation and cytotoxic immune responses, and we propose the HDAC inhibitors as a potential therapeutic strategy for NB patients.

scholarly journals Genetic Variants in the Promoter Region of the Macrophage Migration Inhibitory Factor are Associated with the Severity of Hepatitis C Virus-Induced Liver Fibrosis

2019 ◽  
Vol 20 (15) ◽  
pp. 3753 ◽  
Author(s):  
Wirtz ◽  
Fischer ◽  
Backhaus ◽  
Bergmann ◽  
Brandt ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Liver Fibrosis ◽  
Migration Inhibitory Factor ◽  
Promoter Region ◽  
Macrophage Migration Inhibitory Factor ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Dependent Manner ◽  
Microsatellite Repeats

Two polymorphisms in the promoter region of macrophage migration inhibitory factor (MIF) - rs755622 and rs5844572 - exhibit prognostic relevance in inflammatory diseases. The aim of this study was to investigate a correlation between these MIF promoter polymorphisms and the severity of hepatitis C virus (HCV)-induced liver fibrosis. Our analysis included two independent patient cohorts with HCV-induced liver fibrosis (504 and 443 patients, respectively). The genotype of the single nucleotide polymorphism (SNP) -173 G/C and the repeat number of the microsatellite polymorphism -794 CATT5–8 were determined in DNA samples and correlated with fibrosis severity. In the first cohort, homozygous carriers of the C allele in the rs755622 had lower fibrosis stages compared to heterozygous carriers or wild types (1.25 vs. 2.0 vs. 2.0; p = 0.03). Additionally, ≥7 microsatellite repeats were associated with lower fibrosis stages (<F2) (p = 0.04). Comparable tendencies were observed in the second independent cohort, where fibrosis was assessed using transient elastography. However, once cirrhosis had been established, the C/C genotype and higher microsatellite repeats correlated with impaired liver function and a higher prevalence of hepatocellular carcinoma. Our study demonstrates that specific MIF polymorphisms are associated with disease severity and complications of HCV-induced fibrosis in a stage- and context-dependent manner.

scholarly journals Redox-dependent Structure and Dynamics of Macrophage Migration Inhibitory Factor Reveal Sites of Latent Allostery

2021 ◽  
Author(s):  
Erin Skeens ◽  
Meagan M Gadzuk-Shea ◽  
Dilip Shah ◽  
Vineet Bhandari ◽  
Devin K Schweppe ◽  
...  
Keyword(s):  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Mutational Analysis ◽  
Redox Conditions ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Dependent Manner ◽  
Structure Based Drug Design ◽  
Cellular Environment ◽  
Wide Range

Macrophage migration inhibitory factor (MIF) is a multifunctional immunoregulatory protein that is a key player in the innate immune response. Given its overexpression at sites of inflammation in a wide range of diseases marked by increasingly oxidative cellular environment, a comprehensive structural understanding of how cellular redox conditions may impact the structure and function of MIF is necessary. We used solution NMR spectroscopy and mass spectrometry to investigate structural and dynamic signatures of MIF under varied solution redox conditions. Our results indicate that the MIF structure is modified and becomes increasingly dynamic in an oxidative environment, which may be a means to alter the MIF functional response in a redox-dependent manner. We identified latent allosteric sites within MIF that are redox-sensitive and mutational analysis reveals that loss of redox-responsive residues attenuates activation of the coreceptor CD74. Leveraging sites of redox-sensitivity therefore reveals an avenue to modulate MIF function in its disease state via structure-based drug design.

scholarly journals Macrophage Migration Inhibitory Factor Promotes the Interaction between the Tumor, Macrophages, and T Cells to Regulate the Progression of Chemically Induced Colitis-Associated Colorectal Cancer

2019 ◽  
Vol 2019 ◽  
pp. 1-16 ◽  
Author(s):  
Thalia Pacheco-Fernández ◽  
Imelda Juárez-Avelar ◽  
Oscar Illescas ◽  
Luis I. Terrazas ◽  
Rogelio Hernández-Pando ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
T Cells ◽  
Intestinal Epithelium ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Chemical Carcinogenesis ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Initial Development ◽  
The Impact

Colitis-associated colorectal cancer (CRC) development has been shown to be related to chronically enhanced inflammation. Macrophage migration inhibitory factor (MIF) is an inflammatory mediator that favors inflammatory cytokine production and has chemotactic properties for the recruitment of macrophages (Møs) and T cells. Here, we investigated the role of MIF in the inflammatory response and recruitment of immune cells in a murine model of chemical carcinogenesis to establish the impact of MIF on CRC genesis and malignancy. We used BALB/c MIF-knockout (MIF-/-) and wild-type (WT) mice to develop CRC by administering intraperitoneal (i.p.) azoxymethane and dextran sodium sulfate in drinking water. Greater tumor burdens were observed in MIF-/- mice than in WT mice. Tumors from MIF-/- mice were histologically identified to be more aggressive than tumors from WT mice. The localization of MIF suggests that it is also involved in cell differentiation. The relative gene expression of il-17, measured by real-time PCR, was higher in MIF-/- CRC mice, compared to the WT CRC and healthy MIF-/- mice. Importantly, compared to the WT intestinal epithelium, lower percentages of tumor-associated Møs were found in the MIF-/- intestinal epithelium. These results suggest that MIF plays a role in controlling the initial development of CRC by attracting Møs to the tumor, which is a condition that favors the initial antitumor responses.

scholarly journals Glioma-derived macrophage migration inhibitory factor (MIF) promotes mast cell recruitment in a STAT5-dependent manner

2013 ◽  
Vol 8 (1) ◽  
pp. 50-58 ◽  
Author(s):  
Jelena Põlajeva ◽  
Tobias Bergström ◽  
Per-Henrik Edqvist ◽  
Anders Lundequist ◽  
Anna Sjösten ◽  
...  
Keyword(s):  
Mast Cell ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Dependent Manner ◽  
Cell Recruitment
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