ArticleAmerican journal of translational research2020
ITK inhibition promotes long-term survival of cardiac allografts by regulating T cell PLCγ phosphorylation.
Article in American journal of translational research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Targeting interleukin-2-inducible T cell kinase ameliorates immune-mediated aplastic anemia.Cancer immunology, immunotherapy : CII · 2025Article
- Zanubrutinib Ameliorates Cardiac Fibrosis and Inflammation Induced by Chronic Sympathetic Activation.Molecules (Basel, Switzerland) · 2023Article
- Targeting ITK signaling for T cell-mediated diseases.iScience · 2021Review
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Authors and funding
8 authors.
Funding
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Abstract
backgroundT cells express interleukin-2 inducible T-cell kinase (ITK), which is an essential modulator of T-cell signaling and function. However, the role of ITK in solid organ transplantation has not been investigated to date. Here, we studied the function of ITK in a murine cardiac transplantation model.
methodMurine heart transplantation was performed using BALB/C mice as donors and C57BL/6 mice as recipients. Subsequent intraperitoneal injections of an ITK-specific inhibitor (BMS-509744) were performed to assess the effects of the kinase following cardiac transplantation. Additionally, naive T cells were isolated to investigate the inhibitor's potential effects in the alloimmune responses.
resultsITK inhibition was found to promote long-term cardiac allograft survival compared with the control group of 36.0 ± 3.8 days vs. 7.0 ± 0.7 days, respectively (
conclusionITK inhibition resulted in lower Th1/Th17 responses after cardiac transplantation and markedly prolonged the mean survival time of the cardiac allografts. Thus, ITK inhibition might be a promising therapeutic target to alleviate alloimmune responses in the cardiac transplantation.
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33042455PMC7540118What OpenQuestion holds
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