c-MAF, a Swiss Army Knife for Tolerance in Lymphocytes

Imbratta, Claire; Hussein, Hind; Andris, Fabienne; Verdeil, Grégory

doi:10.3389/fimmu.2020.00206

Cited by 54 publications

(45 citation statements)

References 126 publications

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“…Another key target of miR-221 and miR-222 is Maf (protein c-Maf). Th17 cells express this transcription factor highly, and it is critical for several important aspects of Th17 differentiation and function (reviewed in Imbratta et al, 2020). In miR-221/222-KO mice, c-Maf expression was enhanced in Th17 cells and not naive, Th1, or Treg fractions isolated from the gut.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-221 and -222 modulate intestinal inflammatory Th17 cell response as negative feedback regulators downstream of interleukin-23

et al. 2021

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Section: Discussionmentioning

confidence: 99%

MicroRNA-221 and -222 modulate intestinal inflammatory Th17 cell response as negative feedback regulators downstream of interleukin-23

et al. 2021

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“…Studies have shown that Maf, and its human ortholog, MAF, are decreased in mouse and human Th1 cells, respectively [14,32]. Ectopic expression of Maf in mature Th1 cells granted them the ability to decrease their production of IFN-γ, thus dampening their pathogenic immune response [16,33]. To determine the effect of MAF on IFNG allows us to better understand the role of MAFTRR.…”

Section: Discussionmentioning

confidence: 99%

Elevated Expression of the Long Noncoding RNA MAFTRR in Patients with Hashimoto’s Thyroiditis

Peng

Ding

et al. 2021

Journal of Immunology Research

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Background. Long noncoding RNAs (lncRNAs) represent an important novel class of noncoding RNA molecule greater than 200 nucleotides that play a key role in the regulation of autoimmune diseases. Previous studies have demonstrated that MAFTRR (MAF transcriptional regulator RNA) regulated Th1 cells differentiation by inhibiting the expression of MAF in activated CD4+ T cells. However, the effect of MAFTRR on the pathogenesis of Hashimoto’s thyroiditis (HT) remains unclear. This research was aimed at investigating the expression of MAFTRR in Hashimoto’s thyroiditis (HT) as well as the correlation between MAFTRR and Th1 cells. Methods. Thirty-eight HT patients and thirty-eight healthy controls were enrolled in the study. The proportion of Th1 cells and CD8+IFN-γ+ T cells in peripheral blood mononuclear cells (PBMCs) from these specimens was determined by flow cytometric analysis. The transcript levels of MAFTRR, MAF, and IFNG in PBMCs and thyroid glands were detected by quantitative real-time PCR. Receiver operating characteristic (ROC) curve analysis was performed to evaluate the potential value of MAFTRR in the HT patients. Results. We found that the proportion of circulating Th1 cells and the transcript levels of IFNG were increased in peripheral blood of the HT patients. The transcript levels of MAFTRR were significantly increased in the HT patients and positively correlated with the percentage of Th1 cells and serum levels of antithyroglobulin antibody and antithyroperoxidase antibody. The transcript levels of MAF, a transcription factor that inhibits Th1 cells activity and IFN-γ production, were attenuated in PBMCs from the HT patients. The transcript levels of IFNG had positive and inverse correlations with MAFTRR and MAF expression in PBMCs from the HT patients, respectively. Additionally, a significantly positive correlation between upregulated MAFTRR expression and augmented IFNG expression was revealed in thyroid tissues from the HT patients. ROC curve suggested that MAFTRR could potentially differentiate the HT patients from healthy controls. Conclusion. MAFTRR is significantly augmented in the HT patients and may contribute to the pathogenic role of the Th1 cells response in HT.

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“…Subsequently it was reported to be a transcription factor essential for IL-4 expression in helper T (Th) cells of the immune system [ 40 ]. Since then, it has been reported to be important for regulating the functions of various immune cells, in particular T cells [ 41 ] and functional analysis of it in the immune system has progressed. We generated c-Maf -deficient mice to elucidate its functions in other organs [ 42 ].…”

Section: Functional Analysis Of Large Maf Transcription Factors In Vivomentioning

confidence: 99%

Functional analysis of large MAF transcription factors and elucidation of their relationships with human diseases

Takahashi

2021

Exp. Anim.

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The large MAF transcription factor group is a group of transcription factors with an acidic region, a basic region, and a leucine zipper region. Four types of MAF, MAFA, MAFB, c-MAF, and NRL, have been identified in humans and mice. In order to elucidate the functions of the large MAF transcription factor group in vivo , our research group created genetically modified MAFA-, MAFB-, and c-MAF-deficient mice and analyzed their phenotypes. MAFA is expressed in pancreatic β cells and is essential for insulin transcription and secretion. MAFB is essential for the development of pancreatic endocrine cells, formation of inner ears, podocyte function in the kidneys, and functional differentiation of macrophages. c-MAF is essential for lens formation and osteoblast differentiation. Furthermore, a single-base mutation in genes encoding the large MAF transcription factor group causes congenital renal disease, eye disease, bone disease, diabetes, and tumors in humans. This review describes the functions of large MAF transcription factors in vivo and their relationships with human diseases.

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c-MAF, a Swiss Army Knife for Tolerance in Lymphocytes

Cited by 54 publications

References 126 publications

MicroRNA-221 and -222 modulate intestinal inflammatory Th17 cell response as negative feedback regulators downstream of interleukin-23

MicroRNA-221 and -222 modulate intestinal inflammatory Th17 cell response as negative feedback regulators downstream of interleukin-23

Elevated Expression of the Long Noncoding RNA MAFTRR in Patients with Hashimoto’s Thyroiditis

Functional analysis of large MAF transcription factors and elucidation of their relationships with human diseases

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