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Induction and Regulation of Autoimmunity

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 June 2018) | Viewed by 4648

Special Issue Editor

Department of Microbiology and Immunology, University of Maryland School of Medicine, 685 W. Baltimore Street, HSF-1, Suite 380, Baltimore, MD 21201, USA
Interests: autoimmunity; targeted therapy; natural products
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Autoimmune diseases result from unabated immune responses to self-antigens following a break in immune tolerance leading to tissue dysfunction and damage. Both genetic and environmental factors are involved in the pathogenesis of autoimmunity. Several autoimmune diseases show an association with particular major histocompatibility complex (MHC) haplotypes. In addition, non-MHC genes have also been shown to influence susceptibility/resistance to autoimmunity. The environmental factors comprise diverse agents and stimuli, including external microbes, smoke and other toxic substances. The outcome of the interactions between genetic and environmental factors can be further modulated by stress. In addition, the impact of microbial flora and metabolic factors on autoimmune pathogenesis is becoming increasingly clear. The activity of pathogenic effector lymphoid cells can be controlled by a variety of regulatory T cells. Furthermore, some of the above-mentioned factors that are implicated in the induction of autoimmunity can, under different circumstances, also mediate regulatory activities, thus emphasizing the dual role of some of the mediators of autoimmunity. Strategies aimed at inhibiting the generation and expansion of pathogenic effector cells and/or enhancing the induction and activity of regulatory cells are being extensively pursued for the prevention and treatment of autoimmunity. Stem cell research is adding a new dimension to the therapeutic arsenal against these diseases. This Special Issue is devoted to the elaboration of cellular and molecular mechanisms underlying the induction and regulation of autoimmunity, as well as novel therapeutic approaches for the control of autoimmunity. Both original and review articles covering these aspects of autoimmunity are welcome.

Prof. Dr. Kamal D. Moudgil
Guest Editor

Manuscript Submission Information

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Keywords

  • Autoantigens
  • Autoantibodies
  • Autoimmunity
  • Immunoregulation
  • Immunotherapy
  • Major histocompatibility complex
  • Metabolomics
  • Microbial flora
  • Regulatory cells
  • Self-tolerance
  • T helper cells

Published Papers (1 paper)

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Research

14 pages, 15925 KiB  
Article
lncRNA NTT/PBOV1 Axis Promotes Monocyte Differentiation and Is Elevated in Rheumatoid Arthritis
by Chin-An Yang, Ju-Pi Li, Ju-Chen Yen, I-Lu Lai, Yu-Chen Ho, Yu-Chia Chen, Joung-Liang Lan and Jan-Gowth Chang
Int. J. Mol. Sci. 2018, 19(9), 2806; https://doi.org/10.3390/ijms19092806 - 18 Sep 2018
Cited by 50 | Viewed by 4270
Abstract
Monocytes/macrophages are important in orchestrating inflammatory responses. However, knowledge of the long noncoding RNA (lncRNA) regulation of monocytic cell differentiation and diseases remains limited. We aimed to elucidate the role of the 17 kb lncRNA noncoding transcript in T cells (NTT) [...] Read more.
Monocytes/macrophages are important in orchestrating inflammatory responses. However, knowledge of the long noncoding RNA (lncRNA) regulation of monocytic cell differentiation and diseases remains limited. We aimed to elucidate the role of the 17 kb lncRNA noncoding transcript in T cells (NTT) in monocyte functions. Knockdown and chromatin immunoprecipitation (ChIP) assays in THP-1 cells (human monocytic leukemia cell line) revealed that NTT is regulated by the monocyte key transcription factor C/EBPβ and that it binds to the promoter of nearby gene PBOV1 via hnRNP-U. Overexpression of PBOV1 in THP-1 cells resulted in cell cycle G1 arrest, differentiation into macrophages, a marked increase in IL-10 and CXCL10 mRNA levels, and upregulation of the costimulatory molecules. In contrast to the downregulated NTT observed in lipopolysaccharide (LPS)-treated THP-1 cells, the C/EBPβ/NTT/PBOV1 axis was found to be hyperactivated in peripheral blood mononuclear cells (PBMCs) of first-time diagnosed untreated early rheumatoid arthritis (RA) patients, and their gene expression levels decreased markedly after treatment. Higher initial C/EBPβ/NTT/PBOV1 expression levels were associated with a trend of higher disease activity DAS28 scores. In conclusion, our study suggests that the lncRNA NTT is a regulator of inflammation in monocytes, and its activation participates in monocyte/macrophage differentiation and the pathogenesis of RA. Full article
(This article belongs to the Special Issue Induction and Regulation of Autoimmunity)
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