Febrile Temperature Critically Controls the Differentiation and Pathogenicity of T Helper 17 Cells

Wang, Xiaohu; Ni, L.; Wan, Siyuan; Zhao, Xiaohong; Ding, Xiao; Dejean, Anne; Dong, Chen

doi:10.1016/j.immuni.2020.01.006

Cited by 65 publications

(55 citation statements)

References 56 publications

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“…PIGF is also required for the progression of collagen-induced arthritis in mice ( 105 ). Th17 cell differentiation program is highly heterogeneous ( 106 ) and is controlled by numerous factors, including febrile temperature ( 107 ). The fever shapes Th17 cell differentiation by SUMOylation of the transcription factor SMAD4 ( 107 ), which is tightly associated with T cell function during inflammation ( 108 , 109 ).…”

Section: The Role and Mechanisms Of T Cells In Fibrosis And Fibrotic mentioning

confidence: 99%

“…Th17 cell differentiation program is highly heterogeneous ( 106 ) and is controlled by numerous factors, including febrile temperature ( 107 ). The fever shapes Th17 cell differentiation by SUMOylation of the transcription factor SMAD4 ( 107 ), which is tightly associated with T cell function during inflammation ( 108 , 109 ). SMAD4 has been reported to control Th17 function with an oncoprotein SKI ( 110 , 111 ), which has been linked to wound healing and fibrosis ( 112 ).…”

Section: The Role and Mechanisms Of T Cells In Fibrosis And Fibrotic mentioning

confidence: 99%

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T Cells in Fibrosis and Fibrotic Diseases

2020

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Fibrosis is the extensive deposition of fibrous connective tissue, and it is characterized by the accumulation of collagen and other extracellular matrix (ECM) components. Fibrosis is essential for wound healing and tissue repair in response to a variety of triggers, which include infection, inflammation, autoimmune disorder, degenerative disease, tumor, and injury. Fibrotic remodeling in various diseases, such as liver cirrhosis, pulmonary fibrosis, renal interstitial fibrosis, myocardial infarction, systemic sclerosis (SSc), and graft-versus-host disease (GVHD), can impair organ function, causing high morbidity and mortality. Both innate and adaptive immunity are involved in fibrogenesis. Although the roles of macrophages in fibrogenesis have been studied for many years, the underlying mechanisms concerning the manner in which T cells regulate fibrosis are not completely understood. The T cell receptor (TCR) engages the antigen and shapes the repertoire of antigen-specific T cells. Based on the divergent expression of surface molecules and cell functions, T cells are subdivided into natural killer T (NKT) cells, γδ T cells, CD8 + cytotoxic T lymphocytes (CTL), regulatory T (Treg) cells, T follicular regulatory (Tfr) cells, and T helper cells, including Th1, Th2, Th9, Th17, Th22, and T follicular helper (Tfh) cells. In this review, we summarize the pro-fibrotic or anti-fibrotic roles and distinct mechanisms of different T cell subsets. On reviewing the literature, we conclude that the T cell regulations are commonly disease-specific and tissue-specific. Finally, we provide perspectives on microbiota, viral infection, and metabolism, and discuss the current advancements of technologies for identifying novel targets and developing immunotherapies for intervention in fibrosis and fibrotic diseases.

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Section: The Role and Mechanisms Of T Cells In Fibrosis And Fibrotic mentioning

confidence: 99%

Section: The Role and Mechanisms Of T Cells In Fibrosis And Fibrotic mentioning

confidence: 99%

T Cells in Fibrosis and Fibrotic Diseases

2020

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“…8,[12][13][14][15][16][17][18][19] Recently, fever induced T H 17 cells were also shown to induce expression of transcription factors involved in induction of EAE. 86 IL17 is also known to have a negative effect on the proliferation of hepatitis B virus-related hepatocellular carcinoma. 87 Further, IL17 has been implicated in different types of human cancers 88,89 and may contribute to HBV-associated liver diseases.…”

Section: Discussionmentioning

confidence: 99%

Role of T_H17 Responses in Increasing Herpetic Keratitis in the Eyes of Mice Infected with HSV-1

Hirose

Jaggi

Wang

et al. 2020

Invest. Ophthalmol. Vis. Sci.

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PURPOSE. T H 17 cells play an important role in host defense and autoimmunity yet very little is known about the role of IL17 in herpes simplex virus (HSV)-1 infectivity. To better understand the relationship between IL17 and HSV-1 infection, we assessed the relative impact of IL17A-deficiency and deficiency of its receptors on HSV-1 responses in vivo. METHODS. We generated IL17RA −/− and IL17RA −/− RC −/− mice in-house and infected them along with IL17A −/− and IL17RC −/− mice in the eyes with 2 × 10 5 PFU/eye of wild type (WT) HSV-1 strain McKrae. WT C57BL/6 mice were used as control. Virus replication in the eye, survival, corneal scarring (CS), angiogenesis, levels of latency-reactivation, and levels of CD8 and exhaustion markers (PD1, TIM3, LAG3, CTLA4, CD244, and CD39) in the trigeminal ganglia (TG) of infected mice were determined on day 28 postinfection. RESULTS. No significant differences in virus replication in the eye, survival, latency, reactivation, and exhaustion markers were detected among IL17A −/− , IL17RA −/− , IL17RC −/− , IL17RA −/− RC −/− , and WT mice. However, mice lacking IL17 had significantly less CS and angiogenesis than WT mice. In addition, angiogenesis levels in the absence of IL17RC and irrespective of the absence of IL17RA were significantly less than in IL17A-or IL17RAdeficient mice. CONCLUSIONS. Our results suggest that the absence of IL17 protects against HSV-1-induced eye disease, but has no role in protecting against virus replication, latency, or reactivation. In addition, our data provide rationale for blocking IL17RC function rather than IL17A or IL17RA function as a key driver of HSV-1-induced eye disease.

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“…Accumulative evidence indicated that Th17 cells differentiated by IL-6 and TGFβ1 displayed nonpathogenic but regulatory phenotype with increased IL-10 expression, while Th17 cells generated in the surrounding environments containing IL-1β, IL-23, and salt, serum amyloid A, showed increased pathogenenicity. [35][36][37][38] This probably was the main reason why Th17 cells generated in the presence or absence of IL-1β showed a different effect on corneal allograft rejection. Overall, these results indicated that IL-1β potentiated corneal allograft rejection through boosting Th17 cell differentiation or pathogenicity, at least in part.…”

Section: Nlrp3 Inflammasome-derived Il-1β Aggravated Corneal Allogrmentioning

confidence: 99%

The NLRP3 inflammasome regulates corneal allograft rejection through enhanced phosphorylation of STAT3

Wei

Chi

et al. 2020

American Journal of Transplantation

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Keratoplasty is an important therapeutic approach to many corneal disorders, 1,2 and a large body of evidence has demonstrated that grafts placed in uninflamed or "low-risk" host beds enjoy a higher survival rate, thanks in large part to the cornea's immune privilege. 2-4 However, transplantation failure due to allograft rejection remains a major threat to all transplants, particularly following transplantation into inflamed or "high-risk" host beds, 4,5 where survival rates can fall well below 50% despite local immune suppression. 6,7 A better understanding of the pathogenesis of allograft rejection might therefore help to improve patients' outcomes after corneal transplantations. NOD, LRR-and pyrin domain-containing protein3 (NLRP3) is an intracellular sensor that can detect a broad range of microbial motifs, endogenous danger signals, and environmental irritants, in response to which NLRP3 inflammasomes are then formed and activated. 8,9 The activated NLRP3 inflammasomes results in a

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Febrile Temperature Critically Controls the Differentiation and Pathogenicity of T Helper 17 Cells

Cited by 65 publications

References 56 publications

T Cells in Fibrosis and Fibrotic Diseases

T Cells in Fibrosis and Fibrotic Diseases

Role of T_H17 Responses in Increasing Herpetic Keratitis in the Eyes of Mice Infected with HSV-1

The NLRP3 inflammasome regulates corneal allograft rejection through enhanced phosphorylation of STAT3

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Febrile Temperature Critically Controls the Differentiation and Pathogenicity of T Helper 17 Cells

Cited by 65 publications

References 56 publications

T Cells in Fibrosis and Fibrotic Diseases

T Cells in Fibrosis and Fibrotic Diseases

Role of TH17 Responses in Increasing Herpetic Keratitis in the Eyes of Mice Infected with HSV-1

The NLRP3 inflammasome regulates corneal allograft rejection through enhanced phosphorylation of STAT3

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Product

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Role of T_H17 Responses in Increasing Herpetic Keratitis in the Eyes of Mice Infected with HSV-1