NDLI: RKIP contributes to IFNγ synthesis by CD8+ T cells after serial TCR triggering in Systemic Inflammatory Response Syndrome

Content Provider	PubMed Central
Author	Wright, Kyle T. Vella, Anthony T.
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 which utilizes staphylococcal enterotoxin A (SEA) specific for Vβ3+ T cells, we show that RKIP is necessary for the exaggerated production of IFNγ 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 T cell receptor in SEA-specific CD8+ T cells. Importantly, mice lacking RKIP were still able to proliferate, survive, and contribute to cytokine production in response to PAMP-TLR mediated stimuli, despite the TCR-dependent defects seen in our SIRS model. Finally, by blocking RKIP in wild type SIRS splenocytes, the IFNγ 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.
Related Links	http://dx.doi.org/10.4049/jimmunol.1203486
Ending Page	716
Page Count	9
Starting Page	708
File Format	PDF
ISSN	00221767
e-ISSN	15506606
Journal	Journal of immunology (Baltimore, Md. : 1950)
Issue Number	2
Volume Number	191
Language	English
Publisher Date	2013-07-15
Access Restriction	Open
Subject Keyword	Medicine(all) Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
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