T-cell-specific Sel1L deletion exacerbates EAE by promoting Th1/Th17-cell differentiation

Xue, Yan; Wu, Yi; Xiao, Tengfei; Zhao, Chuanxiang; Gao, Feng-Wei; Liu, Shuo; Tao, Zehua; Jiang, Yalan; Chen, Shaodan; Ye, Jun; Chen, Hua; Long, Qiaoming; Wang, Hui; Zhou, Xiaoming; Shao, Qixiang; Qi, Ling; Sheng, Xia

doi:10.1016/j.molimm.2022.06.001

Cited by 6 publications

(8 citation statements)

References 50 publications

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“…87 In our previous study, we also found that Sel1L deficiency in CD4 + T cells promoted the differentiation of Th1 and Th17 cells in vitro and aggravated the severity of experimental autoimmune encephalomyelitis (EAE). 82 In a T cell-specific Hrd1 knockout mouse model (Hrd1 flox/flox ; CD4-cre mice), Hrd1 did not appear to regulate cytokine production in CD4 + T cells through the ubiquitination and degradation activities of p27kip1. Loss of p27kip1 in the specifically Hrd1 deficient T cells could rescue T cell proliferation but the production of IL-2, IFN-γ, and IL-17 was not restored.…”

Section: Activation and Differentiationmentioning

confidence: 96%

“…81 Similarly, in a T cell-specific Sel1L knockout mouse model (Sel1L flox/flox ; LCK-Cre mice), Sel1L deletion influenced the development of thymocytes at the DN3 stage. 82 Hrd1 conditional deletion in T cells (Hrd1 flox/flox ; CD4-Cre mice) induces abnormal development of thymocytes and lowers the number of lymphocytes in the thymus and spleen. Moreover, Hrd1 increases T cells proliferation by deleting p27kip1 protein.…”

Section: Erad In T Cell Developmentmentioning

confidence: 99%

“…83 However, in the EAE model of T cell-specific Sel1L knockout mice (Sel1L flox/flox ; LCK-Cre mice), increased Th1 and Th17 cells appeared in the central and peripheral organs, indicating that the specific deletion of Sel1L in T cells promotes Th1/ Th17-mediated inflammation. 82 This indicates that ERAD may play a different role in MS. In an EAE model of T cell-specific knockout of BECN1 mice (BECN1 flox/flox ; CD4-Cre mice), the number of IFN-γ + CD4 + T cells decreased significantly, suggesting that blocking autophagy results in the resistance to EAE induction.…”

Section: Multiple Sclerosismentioning

confidence: 99%

“…Specific deletion of Sel1L in T cells promotes Th1/ Th17-mediated inflammation. [82] 4. Blocking autophagy results in the resistance of EAE induction.…”

Section: T-cell-mediated Diseasesmentioning

confidence: 99%

“…In the ETP conditional knockout Sel1L mouse model (Sel1Lflox/flox; CD2‐Cre mice), the lack of Sel1L promotes the apoptosis of thymocytes following β selection and impairs the transition from DN3 to DN4 in mouse αβ T cells 81 . Similarly, in a T cell‐specific Sel1L knockout mouse model (Sel1L flox/flox ; LCK‐Cre mice), Sel1L deletion influenced the development of thymocytes at the DN3 stage 82 . Hrd1 conditional deletion in T cells (Hrd1 flox/flox ; CD4‐Cre mice) induces abnormal development of thymocytes and lowers the number of lymphocytes in the thymus and spleen.…”

Section: Er Stress In the Development Of T Cellsmentioning

confidence: 99%

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Endoplasmic reticulum stress in T cell‐mediated diseases

Chen

Wang

et al. 2023

Scand J Immunol

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T cells synthesize a large number of proteins during their development, activation, and differentiation. The build‐up of misfolded and unfolded proteins in the endoplasmic reticulum, however, causes endoplasmic reticulum (ER) stress. Thus, T cells can maintain ER homeostasis via endoplasmic reticulum‐associated degradation, unfolded protein response, and autophagy. In T cell‐mediated diseases, such as rheumatoid arthritis, systemic lupus erythematosus, Sjogren's syndrome, type 1 diabetes and vitiligo, ER stress caused by changes in the internal microenvironment can cause disease progression by affecting T cell homeostasis. This review discusses ER stress in T cell formation, activation, differentiation, and T cell‐mediated illnesses, and may offer new perspectives on the involvement of T cells in autoimmune disorders and cancer.

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Section: Activation and Differentiationmentioning

confidence: 96%

Section: Erad In T Cell Developmentmentioning

confidence: 99%

Section: Multiple Sclerosismentioning

confidence: 99%

“…Specific deletion of Sel1L in T cells promotes Th1/ Th17-mediated inflammation. [82] 4. Blocking autophagy results in the resistance of EAE induction.…”

Section: T-cell-mediated Diseasesmentioning

confidence: 99%

Section: Er Stress In the Development Of T Cellsmentioning

confidence: 99%

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Endoplasmic reticulum stress in T cell‐mediated diseases

Chen

Wang

et al. 2023

Scand J Immunol

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Casting Light on the Janus-Faced HMG-CoA Reductase Degradation Protein 1: A Comprehensive Review of Its Dualistic Impact on Apoptosis in Various Diseases

Moghadam,

Daraei,

Haddadi

et al. 2024

Mol Neurobiol

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Genetic disruption of mammalian endoplasmic reticulum‐associated protein degradation: Human phenotypes and animal and cellular disease models

Badawi

Mohamed

Varghese

et al. 2023

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Endoplasmic reticulum-associated protein degradation (ERAD) is a stringent quality control mechanism through which misfolded, unassembled and some native proteins are targeted for degradation to maintain appropriate cellular and organelle homeostasis. Several in vitro and in vivo ERAD-related studies have provided mechanistic insights into ERAD pathway activation and its consequent events; however, a majority of these have investigated the effect of ERAD substrates and their consequent diseases affecting the degradation process. In this review, we present all reported human single-gene disorders caused by genetic variation in genes that encode ERAD components rather than their substrates. Additionally, after extensive literature survey, we present various genetically manipulated higher cellular and mammalian animal models that lack specific components involved in various stages of the ERAD pathway.

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T-cell-specific Sel1L deletion exacerbates EAE by promoting Th1/Th17-cell differentiation

Cited by 6 publications

References 50 publications

Endoplasmic reticulum stress in T cell‐mediated diseases

Endoplasmic reticulum stress in T cell‐mediated diseases

Casting Light on the Janus-Faced HMG-CoA Reductase Degradation Protein 1: A Comprehensive Review of Its Dualistic Impact on Apoptosis in Various Diseases

Genetic disruption of mammalian endoplasmic reticulum‐associated protein degradation: Human phenotypes and animal and cellular disease models

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