Dichloroacetate induces regulatory T-cell differentiation and suppresses Th17-cell differentiation by pyruvate dehydrogenase kinase-independent mechanism

2016 ◽  
Vol 69 (1) ◽  
pp. 43-51 ◽  
Author(s):  
Naoyuki Makita ◽  
Jun Ishiguro ◽  
Keisuke Suzuki ◽  
Futoshi Nara
Keyword(s):  
Cell Differentiation ◽  
T Cell ◽  
Pyruvate Dehydrogenase ◽  
Regulatory T Cell ◽  
Th17 Cell ◽  
T Cell Differentiation ◽  
Pyruvate Dehydrogenase Kinase ◽  
Th17 Cell Differentiation ◽  
Independent Mechanism

scholarly journals Protein Kinase CK2 Controls the Fate between Th17 Cell and Regulatory T Cell Differentiation

2017 ◽  
Vol 198 (11) ◽  
pp. 4244-4254 ◽  
Author(s):  
Sara A. Gibson ◽  
Wei Yang ◽  
Zhaoqi Yan ◽  
Yudong Liu ◽  
Amber L. Rowse ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
T Cell ◽  
Protein Kinase ◽  
Regulatory T Cell ◽  
Th17 Cell ◽  
Protein Kinase Ck2 ◽  
T Cell Differentiation ◽  
Kinase Ck2

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.

scholarly journals Requirement for CD28 in Effector Regulatory T Cell Differentiation, CCR6 Induction, and Skin Homing

2015 ◽  
Vol 195 (9) ◽  
pp. 4154-4161 ◽  
Author(s):  
Ruan Zhang ◽  
Christopher M. Borges ◽  
Martin Y. Fan ◽  
John E. Harris ◽  
Laurence A. Turka
Keyword(s):  
Cell Differentiation ◽  
T Cell ◽  
Regulatory T Cell ◽  
T Cell Differentiation ◽  
Skin Homing

scholarly journals HTLV-1 induces T cell malignancy and inflammation by viral antisense factor-mediated modulation of the cytokine signaling

2020 ◽  
Vol 117 (24) ◽  
pp. 13740-13749 ◽  
Author(s):  
Yusuke Higuchi ◽  
Jun-ichirou Yasunaga ◽  
Yu Mitagami ◽  
Hirotake Tsukamoto ◽  
Kazutaka Nakashima ◽  
...  
Keyword(s):  
T Cells ◽  
Cell Differentiation ◽  
T Cell ◽  
Transgenic Mice ◽  
Regulatory T Cell ◽  
T Cell Differentiation ◽  
Cytokine Signaling ◽  
Viral Gene ◽  
Cell Leukemia Virus Type ◽  
Human T Cell

Human T cell leukemia virus type 1 (HTLV-1) is the etiologic agent of a T cell neoplasm and several inflammatory diseases. A viral gene, HTLV-1 bZIP factor (HBZ), induces pathogenic Foxp3-expressing T cells and triggers systemic inflammation and T cell lymphoma in transgenic mice, indicating its significance in HTLV-1–associated diseases. Here we show that, unexpectedly, a proinflammatory cytokine, IL-6, counteracts HBZ-mediated pathogenesis. Loss of IL-6 accelerates inflammation and lymphomagenesis in HBZ transgenic mice. IL-6 innately inhibits regulatory T cell differentiation, suggesting that IL-6 functions as a suppressor against HBZ-associated complications. HBZ up-regulates expression of the immunosuppressive cytokine IL-10. IL-10 promotes T cell proliferation only in the presence of HBZ. As a mechanism of growth promotion by IL-10, HBZ interacts with STAT1 and STAT3 and modulates the IL-10/JAK/STAT signaling pathway. These findings suggest that HTLV-1 promotes the proliferation of infected T cells by hijacking the machinery of regulatory T cell differentiation. IL-10 induced by HBZ likely suppresses the host immune response and concurrently promotes the proliferation of HTLV-1 infected T cells.

Sign in / Sign up

Export Citation Format

Share Document