Induction of thymocyte apoptosis in mice by Yersinia enterocolitica products

Lin, Yee‐Shin; Chen, K.-H.; Kuo, Chih Feng; Huang, Kuen-Jeng; Wu, Jiunn Jong

doi:10.1099/00222615-47-5-447

Cited by 2 publications

(2 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…102180). The mice were given a lethal overdose of pentobarbital (200 mg/kg, intraperitoneal), and their thymic tissue was harvested according to previous work [ 18 ]. Mouse thymocytes were carefully layered over Histopaque-1083 (Sigma-Aldrich) and centrifuged at 400× g for 30 min at 20 °C in a swinging-bucket centrifuge without braking.…”

Section: Methodsmentioning

confidence: 99%

Glycogen Synthase Kinase-3β Facilitates Cytokine Production in 12-O-Tetradecanoylphorbol-13-Acetate/Ionomycin-Activated Human CD4+ T Lymphocytes

Tsai

Tseng

et al. 2020

Cells

View full text Add to dashboard Cite

Cytokines are the major immune regulators secreted from activated CD4+ T lymphocytes that activate adaptive immunity to eradicate nonself cells, including pathogens, tumors, and allografts. The regulation of glycogen synthase kinase (GSK)-3β, a serine/threonine kinase, controls cytokine production by regulating transcription factors. The artificial in vitro activation of CD4+ T lymphocytes by a combination of 12-O-tetradecanoylphorbol-13-acetate and ionomycin, the so-called T/I model, led to an inducible production of cytokines, such as interferon-γ, tumor necrosis factor-α, and interleukin-2. As demonstrated by the approaches of pharmacological targeting and genetic knockdown of GSK-3β, T/I treatment effectively caused GSK-3β activation followed by GSK-3β-regulated cytokine production. In contrast, pharmacological inhibition of the proline-rich tyrosine kinase 2 and calcineurin signaling pathways blocked cytokine production, probably by deactivating GSK-3β. The blockade of GSK-3β led to the inhibition of the nuclear translocation of T-bet, a vital transcription factor of T lymphocyte cytokines. In a mouse model, treatment with the GSK-3β inhibitor 6-bromoindirubin-3’-oxime significantly inhibited T/I-induced mortality and serum cytokine levels. In summary, targeting GSK-3β effectively inhibits CD4+ T lymphocyte activation and cytokine production.

show abstract

Section: Methodsmentioning

confidence: 99%

Glycogen Synthase Kinase-3β Facilitates Cytokine Production in 12-O-Tetradecanoylphorbol-13-Acetate/Ionomycin-Activated Human CD4+ T Lymphocytes

Tsai

Tseng

et al. 2020

Cells

View full text Add to dashboard Cite

show abstract

“…Intraperitoneal administration of culture supernates from Yersinia enterocolitica ( Y. enterocolitica ) causes thymocyte apoptosis and increases the proportion of TCRαβ high cells in mice, which is related to the increase in the percentage of cells with high levels of Vβ6 and Vβ8 TCRs ( 79 ). In addition, LPS is not involved in thymic atrophy induced by Y. enterocolitica ( 79 ). The V antigen of Yersinia pestis can interact with receptor-bound human IFN-γ located in thymocytes, triggering thymocyte apoptosis in vitro ( 80 ).…”

Section: Bacteriamentioning

confidence: 99%

Infection-Associated Thymic Atrophy

Ming-li

Qian

et al. 2021

Front. Immunol.

View full text Add to dashboard Cite

The thymus is a vital organ of the immune system that plays an essential role in thymocyte development and maturation. Thymic atrophy occurs with age (physiological thymic atrophy) or as a result of viral, bacterial, parasitic or fungal infection (pathological thymic atrophy). Thymic atrophy directly results in loss of thymocytes and/or destruction of the thymic architecture, and indirectly leads to a decrease in naïve T cells and limited T cell receptor diversity. Thus, it is important to recognize the causes and mechanisms that induce thymic atrophy. In this review, we highlight current progress in infection-associated pathogenic thymic atrophy and discuss its possible mechanisms. In addition, we discuss whether extracellular vesicles/exosomes could be potential carriers of pathogenic substances to the thymus, and potential drugs for the treatment of thymic atrophy. Having acknowledged that most current research is limited to serological aspects, we look forward to the possibility of extending future work regarding the impact of neural modulation on thymic atrophy.

show abstract

Induction of thymocyte apoptosis in mice by Yersinia enterocolitica products

Cited by 2 publications

References 32 publications

Glycogen Synthase Kinase-3β Facilitates Cytokine Production in 12-O-Tetradecanoylphorbol-13-Acetate/Ionomycin-Activated Human CD4+ T Lymphocytes

Glycogen Synthase Kinase-3β Facilitates Cytokine Production in 12-O-Tetradecanoylphorbol-13-Acetate/Ionomycin-Activated Human CD4+ T Lymphocytes

Infection-Associated Thymic Atrophy

Contact Info

Product

Resources

About