ArticleJournal of immunology (Baltimore, Md. : 1950)2013
RKIP contributes to IFN-γ synthesis by CD8+ T cells after serial TCR triggering in systemic inflammatory response syndrome.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- The YYR (YY1- RKIP) Regulatory Axis in the pathogenesis of Cancer and Immune Evasion.Journal of experimental & clinical cancer research : CR · 2025Review
- Unraveling the RKIP-YY1 axis: immune crosstalk in the pathogenesis of metabolic disorders.Frontiers in immunology · 2025Review
- Review
- Antigen-specific downregulation of miR-150 in CD4 T cells promotes cell survival.Frontiers in immunology · 2023Article
- Article
- Raf kinase inhibitory protein reduces bradykinin receptor desensitization.Journal of neurochemistry · 2022Article
- Raf Kinase Inhibitory Protein regulates the cAMP-dependent protein kinase signaling pathway through a positive feedback loop.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Harnessing RKIP to Combat Heart Disease and Cancer.Cancers · 2022Review
- Insights of RKIP-Derived Suppression of Prostate Cancer.Cancers · 2021Review
- Review
- Article
- RKIP as an Inflammatory and Immune System Modulator: Implications in Cancer.Biomolecules · 2019Review
- Article
- Article
- Responses to LPS boost effector CD8 T-cell accumulation outside of signals 1 and 2.Cellular & molecular immunology · 2017Article
- Transition from identity to bioactivity-guided proteomics for biomarker discovery with focus on the PF2D platform.Proteomics. Clinical applications · 2016Review
- Therapeutic targeting of the inflammome.Biochemical pharmacology · 2014Review
- Interactions of RKIP with inflammatory signaling pathways.Critical reviews in oncogenesis · 2014Review
- RKIP structure drives its function: a three-state model for regulation of RKIP.Critical reviews in oncogenesis · 2014Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Systemic inflammatory response syndrome (SIRS) is associated with the development of severe medical complications, including progression to multiple organ dysfunction syndrome and even death. To date, only marginal improvements in terms of therapeutic options have been established for patients affected by SIRS. Raf kinase inhibitor protein (RKIP) is a regulator of MAPK and NF-κB signaling cascades, which are both critical for production of the proinflammatory cytokines responsible for SIRS initiation. By testing a T cell-dependent mouse model of SIRS that utilizes staphylococcal enterotoxin A specific for Vβ3(+) T cells, we show that RKIP is necessary for the exaggerated production of IFN-γ from SIRS splenocytes. This effect was not due to differences in T cell expansion, IL-10 production, or APC priming, but rather a cell-intrinsic defect lying downstream of the TCR in staphylococcal enterotoxin A-specific CD8(+) T cells. Importantly, mice lacking RKIP were still able to proliferate, survive, and contribute to cytokine production in response to pathogen associated molecular pattern-TLR-mediated stimuli, despite the TCR-dependent defects seen in our SIRS model. Finally, by blocking RKIP in wild-type SIRS splenocytes, the IFN-γ response by CD8(+) Vβ3(+) T cells was significantly diminished. These data suggest that RKIP may be a potential therapeutic target in SIRS by curbing effector cytokine production from CD8(+) T cells during serial TCR triggering.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.