The role of metabolism in Th17 cell differentiation and autoimmune diseases

2022 ◽  
Vol 103 ◽  
pp. 108450
Author(s):  
Guang Wang ◽  
Zehong Su ◽  
Hui Li ◽  
Li Xiao ◽  
Chengyue Li ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
Autoimmune Diseases ◽  
Th17 Cell ◽  
Th17 Cell Differentiation

scholarly journals Regulation of Suppressors of Cytokine Signaling as a Therapeutic Approach in Autoimmune Diseases, with an Emphasis on Multiple Sclerosis

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Vinod S. Ramgolam ◽  
Silva Markovic-Plese
Keyword(s):  
Multiple Sclerosis ◽  
Cell Differentiation ◽  
Autoimmune Diseases ◽  
Th17 Cell ◽  
Inflammatory Cells ◽  
Cytokine Signaling ◽  
Rapid Induction ◽  
Th17 Cell Differentiation ◽  
Socs3 Expression ◽  
Attractive Therapeutic Target

Multiple sclerosis (MS) is an inflammatory demyelinating, presumably autoimmune disease of the central nervous system (CNS). Among the available MS therapies, interferon (IFN)β and the recently introduced statins have been reported to exert their immunomodulatory effects through the induction of SOCS1 and SOCS3 in various inflammatory cell subsets. The SOCS proteins negatively regulate cytokine and Toll-like receptors- (TLR-) induced signaling in the inflammatory cells. SOCS1 and SOCS3 have been reported to play an important role in the regulation of Th17-cell differentiation through their effects on the cells of the innate and adaptive immune systems. IFNβ and statins inhibit Th17-cell differentiation directly and indirectly via induction of SOCS1 and SOCS3 expression in monocytes, dendritic cells (DCs), and B-cells. Due to their rapid induction and degradation, and SOCS-mediated regulation of multiple cytokine-signaling pathways, they represent an attractive therapeutic target in the autoimmune diseases, and particularly relapsing remitting (RR) MS.

scholarly journals IL-17A and Th17 Cells in Lung Inflammation: An Update on the Role of Th17 Cell Differentiation and IL-17R Signaling in Host Defense against Infection

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Hsing-Chuan Tsai ◽  
Sharlene Velichko ◽  
Li-Yin Hung ◽  
Reen Wu
Keyword(s):  
Cell Differentiation ◽  
Host Defense ◽  
Th17 Cell ◽  
Th17 Cells ◽  
Critical Role ◽  
Klebsiella Pneumonia ◽  
Antimicrobial Proteins ◽  
Cytokines And Chemokines ◽  
Th17 Cell Differentiation

The significance of Th17 cells and interleukin- (IL-)17A signaling in host defense and disease development has been demonstrated in various infection and autoimmune models. Numerous studies have indicated that Th17 cells and its signature cytokine IL-17A are critical to the airway’s immune response against various bacteria and fungal infection. Cytokines such as IL-23, which are involved in Th17 differentiation, play a critical role in controllingKlebsiella pneumonia(K. pneumonia) infection. IL-17A acts on nonimmune cells in infected tissues to strengthen innate immunity by inducing the expression of antimicrobial proteins, cytokines, and chemokines. Mice deficient in IL-17 receptor (IL-17R) expression are susceptible to infection by various pathogens. In this review, we summarize the recent advances in unraveling the mechanism behind Th17 cell differentiation, IL-17A/IL-17R signaling, and also the importance of IL-17A in pulmonary infection.

scholarly journals RORα enforces stability of the T-helper-17 cell effector program

2020 ◽  
Author(s):  
June-Yong Lee ◽  
Jason A. Hall ◽  
Maria Pokrovskii ◽  
Lina Kroehling ◽  
Lin Wu ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
Th17 Cell ◽  
Th17 Cells ◽  
T Helper ◽  
T Helper 17 ◽  
Enhancer Element ◽  
Peripheral Tissues ◽  
Th17 Cell Differentiation

SummaryT helper 17 (Th17) cells regulate mucosal barrier defenses, but also promote multiple autoinflammatory diseases. Although many molecular determinants of Th17 cell differentiation have been described, the transcriptional programs that sustain Th17 cells in vivo remain obscure. The transcription factor RORγt is critical for Th17 cell differentiation, but a distinct role of the closely-related RORα, which is co-expressed in Th17 cells, is not known. Here we demonstrate that, although dispensable for Th17 cell differentiation, RORα governs optimal Th17 responses in peripheral tissues. Thus, the absence of RORα in T cells led to significant reductions in both RORγt expression and effector function amongst Th17 cells, due to need for cooperative RORα and RORγt binding to a newly-identified Rorc enhancer element that is essential for Th17 lineage maintenance in vivo. Altogether, these data point to a non-redundant role of RORα in Th17 lineage maintenance via reinforcement of the RORγt transcriptional program.

scholarly journals Critical Role of AdipoR1 in Regulating Th17 Cell Differentiation Through Modulation of HIF-1α-Dependent Glycolysis

2020 ◽  
Vol 11 ◽  
Author(s):  
Qian Zhang ◽  
Lei Wang ◽  
Jintao Jiang ◽  
Shiyu Lin ◽  
Aishu Luo ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
Th17 Cell ◽  
Critical Role ◽  
Th17 Cell Differentiation

scholarly journals Cannabinoids drive Th17 cell differentiation in patients with rheumatic autoimmune diseases

2020 ◽  
Author(s):  
Konstantin Kotschenreuther ◽  
Iris Waqué ◽  
Shuaifeng Yan ◽  
Anja Meyer ◽  
Thom Haak ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
Autoimmune Diseases ◽  
Th17 Cell ◽  
Th17 Cell Differentiation

scholarly journals miRNAs Alter T Helper 17 Cell Fate in the Pathogenesis of Autoimmune Diseases

2021 ◽  
Vol 12 ◽  
Author(s):  
Junxia Huang ◽  
Xinzhi Xu ◽  
Ji Yang
Keyword(s):  
Immune Response ◽  
Cell Differentiation ◽  
Autoimmune Diseases ◽  
Cell Fate ◽  
Th17 Cell ◽  
Th17 Cells ◽  
T Helper ◽  
T Helper 17 ◽  
Th17 Cell Differentiation ◽  
And Function

T helper 17 (Th17) cells are characterized by the secretion of the IL-17 cytokine and are essential for the immune response against bacterial and fungal infections. Despite the beneficial roles of Th17 cells, unrestrained IL-17 production can contribute to immunopathology and inflammatory autoimmune diseases, including multiple sclerosis, rheumatoid arthritis, and inflammatory bowel disease. Although these diverse outcomes are directed by the activation of Th17 cells, the regulation of Th17 cells is incompletely understood. The discovery that microRNAs (miRNAs) are involved in the regulation of Th17 cell differentiation and function has greatly improved our understanding of Th17 cells in immune response and disease. Here, we provide an overview of the biogenesis and function of miRNA and summarize the role of miRNAs in Th17 cell differentiation and function. Finally, we focus on recent advances in miRNA-mediated dysregulation of Th17 cell fate in autoimmune diseases.

Role of PI3K/Akt and mTOR complexes in Th17 cell differentiation

2013 ◽  
Vol 1280 (1) ◽  
pp. 30-34 ◽  
Author(s):  
Shigenori Nagai ◽  
Yutaka Kurebayashi ◽  
Shigeo Koyasu
Keyword(s):  
Cell Differentiation ◽  
Th17 Cell ◽  
Th17 Cell Differentiation

scholarly journals Resolvin D5 Modulates Th17/Treg Cell Differentiation and Suppresses Osteoclastogenesis.

2021 ◽  
Author(s):  
Hirotaka Yamada ◽  
Jun Saegusa ◽  
Sho Sendo ◽  
Yo Ueda ◽  
Takaichi Okano ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
T Cell ◽  
Th17 Cell ◽  
T Cell Differentiation ◽  
T Cell Proliferation ◽  
Lipid Mediator ◽  
Resolution Of Inflammation ◽  
Novel Treatment ◽  
Th17 Cell Differentiation

Abstract Resolvins, are specialized pro-resolving mediators (SPMs) derived from n-3 polyunsaturated fatty acids. They contribute actively to the resolution of inflammation, but little is known concerning their role in chronic inflammation, such as in rheumatoid arthritis (RA). Here, we performed lipid mediator (LM) profiling in tissues from the paws of SKG arthritic mice using lipid chromatography (LC) /mass spectrometry (MS) /MS-based LM metabololipidomics. We found elevated levels of SPMs including resolvin D5 (RvD5) in these tissues. Moreover, RvD5 levels were significantly correlated with arthritis disease activity. From experiments to assess the role of RvD5 in the pathology of RA, we concluded that RvD5 suppressed Th17 cell differentiation and facilitated regulatory T cell differentiation, as well as inhibiting CD4+ T cell proliferation. Furthermore, RvD5 attenuated osteoclast (OC) differentiation and interfered with osteoclastogenesis. Targeting the resolution of inflammation could be promising as a novel treatment for RA.

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