Functional MIF promoter haplotypes modulate Th17-related cytokine expression in peripheral blood mononuclear cells from control subjects and rheumatoid arthritis patients

Hernández-Palma, Luis Alexis; García‐Arellano, Samuel; Bucala, Richard; Llamas-Covarrubias, Mara Anaís; Cruz-Mosso, Ulises De la; Cerpa-Cruz, Sergio; Parra‐Rojas, Isela; Plascencia-Hernández, Arturo; Muñoz‐Valle, José Francisco

doi:10.1016/j.cyto.2018.11.014

Cited by 13 publications

(6 citation statements)

References 61 publications

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“…MIF has two functional promoter polymorphisms that increase the transcription of MIF and both are associated with susceptibility to rheumatoid arthritis (176,177). Not coincidentally, the addition of rMIF to RA patient-derived PBMCs increases IL-17 expression to levels similar to that observed with PBMCs from an individual with a high expression MIF polymorphism haplotype (175). Finally, using a murine model of psoriasiform dermatitis induced by IL-23-a critical determinant of Th17 lymphocyte responses (178)-MIFdeficiency resulted in a dramatic reduction of disease progression (179).…”

Section: T Helper 17 (Th17) Cellsmentioning

confidence: 87%

“…Conversely, clinical analysis of circulating cytokines in women with breast cancer found that MIF expression is increased in later stage and more aggressive molecular cancer subtypes and strongly correlates with IL-17 (173). MIF has also been implicated in non-tumor associated IL-17 expression in a variety of autoimmune disorders including Hashimoto's thyroiditis (174) and rheumatoid arthritis (RA) (175) where Th17 responses are well-characterized to drive pro-inflammation.…”

Section: T Helper 17 (Th17) Cellsmentioning

confidence: 99%

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MIF-Dependent Control of Tumor Immunity

Noe

Mitchell

2020

Front. Immunol.

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Initially identified as a T lymphocyte-elicited inhibitor of macrophage motility, macrophage migration inhibitory factor (MIF) has since been found to be expressed by nearly every immune cell type examined and overexpressed in most solid and hematogenous malignant cancers. It is localized to both extracellular and intracellular compartments and physically interacts with more than a dozen different cell surface and intracellular proteins. Although classically associated with and characterized as a mediator of pro-inflammatory innate immune responses, more recent studies demonstrate that, in malignant disease settings, MIF contributes to anti-inflammatory, immune evasive, and immune tolerant phenotypes in both innate and adaptive immune cell types. This review will summarize the studies describing MIF in tumor-specific innate and adaptive immune responses and attempt to reconcile these various pleiotropic functions in normal physiology.

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Section: T Helper 17 (Th17) Cellsmentioning

confidence: 87%

Section: T Helper 17 (Th17) Cellsmentioning

confidence: 99%

MIF-Dependent Control of Tumor Immunity

Noe

Mitchell

2020

Front. Immunol.

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“…In conclusion, our results contribute important new information that MIF participates in the secretion of IL-25, IL-31, and IL-33, which plays an essential role in Th2 polarization. Although we have reported that MIF favors the secretion of cytokines related to the Th1 and Th17 profile [ 34 , 35 ], the present study indicates that MIF could also be associated with the induction of a Th2 profile, which acts as a negative regulatory circuit, trying to counteract the inflammatory processes observed in RA. However, further studies are needed to explain how MIF induces the expression of IL-25, IL-31, and IL-33 at diverse stages of the disease.…”

Section: Discussionmentioning

confidence: 50%

The Novel Role of MIF in the Secretion of IL-25, IL-31, and IL-33 from PBMC of Patients with Rheumatoid Arthritis

et al. 2021

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Rheumatoid arthritis (RA) is an autoimmune inflammatory joint disease with complex pathogenesis associated with cytokine dysregulation. Macrophage migration inhibitory factor (MIF) plays a role in systemic inflammation and joint destruction in RA and could be associated with the secretion of other immune-modulatory cytokines such as IL-25, IL-31, and IL-33. For the above, our main aim was to evaluate the IL-25, IL-31, and IL-33 secretion from recombinant human MIF (rhMIF)-stimulated peripheral blood mononuclear cells (PBMC) of RA patients. The rhMIF and lipopolysaccharide (LPS) plus rhMIF stimuli promote the secretion of IL-25, IL-31, and IL-33 (p < 0.05) from PBMC of RA patients. The study groups, the different stimuli, and the interaction between both showed a statistically significant effect on the secretion of IL-25 (p < 0.05) and IL-31 (p < 0.01). The study of the effect of the RA patient treatments and their interaction with the effect of stimuli did not show an interaction between them. In conclusion, our study generates new evidence for the role of MIF in the secretion of IL-25, IL-31, and IL-33 and its immunomodulatory effect on RA.

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“…What's more, ICBP90 (Yao et al, 2021)and HIF1-α can up-regulate the transcription level of MIF (Welford et al, 2006;Zis et al, 2015;Safi et al, 2020). Expressed in different tissues and cells, MIF acts different roles in many diseases, such as tumors (Du et al, 2013;Fukaya et al, 2016), autoimmune diseases (Hernandez-Palma et al, 2019) and acute organ injury (Djudjaj et al, 2017;Ochi et al, 2017) (Liu et al, 2021). The MIF protein is pre-formed and stored in the cytoplasmic vesicle structure.…”

Section: Basic Biological Functions Of Macrophage Migration Inhibitor...mentioning

confidence: 99%

Macrophage migration inhibitory factor in acute kidneyinjury

Hao

et al. 2022

Front. Physiol.

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Acute kidney injury (AKI) is a complex clinical syndrome with multiple etiologies and pathogenesis, which lacks early biomarkers and targeted therapy. Recently, macrophage migration inhibitory factor (MIF) family protein have received increasing attention owing to its pleiotropic protein molecule character in acute kidney injury, where it performed a dual role in the pathological process. macrophage migration inhibitory factor and macrophage migration inhibitory factor-2 are released into the peripheral circulation when Acute kidney injury occurs and interact with various cellular pathways. On the one hand, macrophage migration inhibitory factor exerts a protective effect in anti-oxidation and macrophage migration inhibitory factor-2 promotes cell proliferation and ameliorates renal fibrosis. On the other hand, macrophage migration inhibitory factor aggravates renal injury as an upstream inflammation factor. Herein, we provide an overview on the biological role and possible mechanisms of macrophage migration inhibitory factor and macrophage migration inhibitory factor-2 in the process of Acute kidney injury and the clinical application prospects of macrophage migration inhibitory factor family proteins as a potential therapeutic target.

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Functional MIF promoter haplotypes modulate Th17-related cytokine expression in peripheral blood mononuclear cells from control subjects and rheumatoid arthritis patients

Cited by 13 publications

References 61 publications

MIF-Dependent Control of Tumor Immunity

MIF-Dependent Control of Tumor Immunity

The Novel Role of MIF in the Secretion of IL-25, IL-31, and IL-33 from PBMC of Patients with Rheumatoid Arthritis

Macrophage migration inhibitory factor in acute kidneyinjury

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