Targeting Th17 cells in immune diseases

Dong, Chen

doi:10.1038/cr.2014.92

Cited by 28 publications

(19 citation statements)

References 12 publications

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“…Inhibiting key effector cytokines critical for Th17 development has shown a concomitant reduction in tissue inflammation and disease progression (43). Furthermore, central to Th17 polarization is the role of IL-21, which can function as an initial differentiating factor or as a critical amplification component during Th17 development (24,44).…”

Section: Discussionmentioning

confidence: 99%

IL-21R signaling is critical for induction of spontaneous experimental autoimmune encephalomyelitis

Lee¹,

Mitsdoerffer²,

Xiao³

et al. 2015

Journal of Clinical Investigation

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Section: Discussionmentioning

confidence: 99%

IL-21R signaling is critical for induction of spontaneous experimental autoimmune encephalomyelitis

Lee¹,

Mitsdoerffer²,

Xiao³

et al. 2015

Journal of Clinical Investigation

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“…T helper 17 (Th17) cells are a highly pro-inammatory lineage of T helper cells dened by their production of interleukin 17 (IL-17). 55 ROR-gt is necessary and sufficient for cytokine IL-17 expression in mouse and human Th17 cells. 55 Given the inhibitory effects of topotecan against ROR-gt, we further investigate whether topotecan affects IL-17 expression in EAE mice.…”

Section: Topotecan Reverses Multiple Sclerosis In Vivomentioning

confidence: 99%

“…55 ROR-gt is necessary and sufficient for cytokine IL-17 expression in mouse and human Th17 cells. 55 Given the inhibitory effects of topotecan against ROR-gt, we further investigate whether topotecan affects IL-17 expression in EAE mice. Of note, ELISA experiments reveal that topotecan treatment signicantly reduces IL-17 production in brain and spinal cords of EAE mice (Fig.…”

Section: Topotecan Reverses Multiple Sclerosis In Vivomentioning

confidence: 99%

Target identification among known drugs by deep learning from heterogeneous networks

et al. 2020

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“…[2][3][4][5] Recent studies have revealed the involvement of various cell populations and cytokines during SS development, which indicates complex mechanisms for the pathogenesis of SS. 6,7 Recently, Th17 cells have been implicated in the pathogenesis of autoimmune diseases, 8 and therapies targeting Th17 cells have exhibited beneficial effects on disease progression. [9][10][11] Increasing evidence also indicates that Th17 cells are important players in the autoimmune inflammation of SS.…”

Section: Introductionmentioning

confidence: 99%

Proteasome inhibition suppresses Th17 cell generation and ameliorates autoimmune development in experimental Sjögren’s syndrome

et al. 2017

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Immunoproteasome activation in immune cells is involved in the modulation of immune responses. Increasing evidence indicates that proteasome inhibitors show beneficial effects in treating autoimmune diseases, but it remains unclear whether proteasome inhibition is an effective approach for suppressing autoimmune development in Sjögren's syndrome (SS). Our previous work has demonstrated a critical role for Th17 cells in the development of experimental SS (ESS) in mice. In this study, we detected high levels of low-molecular-weight protein 7 (LMP7), a key subunit of the immunoproteasome, in Th17 cells from ESS mice. Moreover, treatment with bortezomib (BTZ), a proteasome inhibitor, markedly suppressed Th17 differentiation in both murine and human naive T cells in culture. Furthermore, ESS mice treated with BTZ displayed significantly higher saliva flow rates and a reduction in tissue destruction in the salivary glands compared with vehicle-treated ESS mice. Notably, BTZ-treated ESS mice showed markedly decreased Th17 cells, germinal center B cells and plasma cells in the peripheral lymphoid organs. In addition, adoptively transferred wild type naive CD4 T cells rapidly differentiated into Th17 cells and induced salivary dysfunction in IL-17-deficient mice immunized for ESS induction. However, BTZ treatment profoundly suppressed the donor T-cell-derived Th17 response and ameliorated the reduction in salivary secretion in IL-17-deficient recipient mice. Taken together, our findings demonstrate that proteasome inhibition can effectively ameliorate ESS by suppressing the Th17 response, which may contribute to the development of a novel therapeutic strategy for the treatment of SS.Cellular &Molecular Immunology advance online publication, 10 July 2017; doi:10.1038/cmi.2017.8.

show abstract

Targeting Th17 cells in immune diseases

Cited by 28 publications

References 12 publications

IL-21R signaling is critical for induction of spontaneous experimental autoimmune encephalomyelitis

IL-21R signaling is critical for induction of spontaneous experimental autoimmune encephalomyelitis

Target identification among known drugs by deep learning from heterogeneous networks

Proteasome inhibition suppresses Th17 cell generation and ameliorates autoimmune development in experimental Sjögren’s syndrome

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