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Act1 is a negative regulator in T and B cells via direct inhibition of STAT3

Adaptor for IL-17 receptors (Act1) is known to be crucial for IL-17-mediated immune responses. Here the authors show that Act1 also functions as a negative regulator of T and B cells by direct inhibition of STAT3.

Cun-Jin Zhang
Chenhui Wang
Xiaoxia Li
ResearchOpen Access16 Jul 2018
Nature Communications

Volume: 9, P: 1-14
IL-17 induced NOTCH1 activation in oligodendrocyte progenitor cells enhances proliferation and inflammatory gene expression

NOTCH signalling stimulates oligodendrocyte progenitor cell proliferation but how this regulates demyelinating disease is unclear. Here, the authors show that an IL-17 adaptor protein, Act1, interacts with the C-terminal fragment of NOTCH1 (NICD) to activate cell proliferation and an inflammatory response.

Chenhui Wang
Cun-Jin Zhang
Xiaoxia Li
ResearchOpen Access31 May 2017
Nature Communications

Volume: 8, P: 1-16
TH17 cells promote CNS inflammation by sensing danger signals via Mincle

Mincle is a pattern recognition receptor that senses danger signals in innate immune cells. Here authors show in an experimental autoimmune encephalomyelitis mouse model that tissue damage triggers Mincle signaling on inflammatory helper T cells, leading to inflammasome-mediated IL-1β production and reinforced inflammation.

Quanri Zhang
Weiwei Liu
Xiaoxia Li
ResearchOpen Access03 May 2022
Nature Communications

Volume: 13, P: 1-12
TAGAP instructs Th17 differentiation by bridging Dectin activation to EPHB2 signaling in innate antifungal response

TAGAP gene variants are linked to human autoimmunity. Here the authors identify TAGAP as a Dectin-1 and EphB2-binding protein mediating antifungal innate immune signaling and cytokine production, and demonstrate TAGAP in non-T cells promotes Th17 response in mouse models of infection and autoimmunity.

Jianwen Chen
Ruirui He
Chenhui Wang
ResearchOpen Access20 Apr 2020
Nature Communications

Volume: 11, P: 1-16
Cancer cell-expressed BTNL2 facilitates tumour immune escape via engagement with IL-17A-producing γδ T cells

Cancer cells producing ligands for the immune checkpoint molecules PD-1 and CTLA-4 is an important mechanism of tumour immune resistance. Here authors show that BTNL2 expression on cancer cells generates a dysfunctional tumour immune microenvironment via promoting IL-17A-producing γδ T cells.

Yanyun Du
Qianwen Peng
Chenhui Wang
ResearchOpen Access11 Jan 2022
Nature Communications

Volume: 13, P: 1-16
T cell–intrinsic ASC critically promotes T_H17-mediated experimental autoimmune encephalomyelitis

Inflammasome activation triggers the release of active interleukin 1β (IL-1β). Li and colleagues show that T_H17 cells can release IL-1β upon T cell antigen receptor and ATP stimulation via an ASC–NLPR3–caspase-8 axis, thereby contributing to neuroinflammation.

Bradley N Martin
Chenhui Wang
Xiaoxia Li
Research21 Mar 2016
Nature Immunology

Volume: 17, P: 583-592
MYO1F regulates T-cell activation and glycolytic metabolism by promoting the acetylation of GAPDH

Zhihui Cui
Heping Wang
Chenhui Wang
Research13 Dec 2024
Cellular & Molecular Immunology

Volume: 22, P: 176-190

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Act1 is a negative regulator in T and B cells via direct inhibition of STAT3

IL-17 induced NOTCH1 activation in oligodendrocyte progenitor cells enhances proliferation and inflammatory gene expression

TH17 cells promote CNS inflammation by sensing danger signals via Mincle

TAGAP instructs Th17 differentiation by bridging Dectin activation to EPHB2 signaling in innate antifungal response

Cancer cell-expressed BTNL2 facilitates tumour immune escape via engagement with IL-17A-producing γδ T cells

T cell–intrinsic ASC critically promotes TH17-mediated experimental autoimmune encephalomyelitis

MYO1F regulates T-cell activation and glycolytic metabolism by promoting the acetylation of GAPDH

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T cell–intrinsic ASC critically promotes T_H17-mediated experimental autoimmune encephalomyelitis