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    CD28 and ITK signals regulate autoreactive T cell trafficking

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    Authors
    Jain, Nitya
    Miu, Bing
    Jiang, Jian-kang
    McKinstry, Kai K.
    Prince, Amanda L.
    Swain, Susan L.
    Greiner, Dale L.
    Thomas, Craig J.
    Sanderson, Michael J.
    Berg, Leslie J.
    Kang, Joonso
    Show allShow less
    UMass Chan Affiliations
    Department of Microbiology and Physiological Systems
    Program in Molecular Medicine
    Department of Pathology
    Document Type
    Journal Article
    Publication Date
    2013-12-01
    Keywords
    Animals
    Antigens, CD28
    CHO Cells
    CTLA-4 Antigen
    Cells, Cultured
    Chemotaxis, Leukocyte
    Cricetinae
    Cricetulus
    Female
    Homeostasis
    Male
    Mice
    Mice, Inbred C57BL
    Mice, Inbred NOD
    Mice, Knockout
    Mice, SCID
    Protein-Tyrosine Kinases
    Signal Transduction
    T-Lymphocytes
    Immunology of Infectious Disease
    Immunopathology
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    Link to Full Text
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4005518/
    Abstract
    Activation of self-reactive T cells and their trafficking to target tissues leads to autoimmune organ destruction. Mice lacking the co-inhibitory receptor cytotoxic T lymphocyte antigen-4 (CTLA-4) develop fatal autoimmunity characterized by lymphocytic infiltration into nonlymphoid tissues. Here, we demonstrate that the CD28 co-stimulatory pathway regulates the trafficking of self-reactive Ctla4(-/-) T cells to tissues. Concurrent ablation of the CD28-activated Tec family kinase ITK does not block spontaneous T cell activation but instead causes self-reactive Ctla4(-/-) T cells to accumulate in secondary lymphoid organs. Despite excessive spontaneous T cell activation and proliferation in lymphoid organs, Itk(-/-); Ctla4(-/-) mice are otherwise healthy, mount antiviral immune responses and exhibit a long lifespan. We propose that ITK specifically licenses autoreactive T cells to enter tissues to mount destructive immune responses. Notably, ITK inhibitors mimic the null mutant phenotype and also prevent pancreatic islet infiltration by diabetogenic T cells in mouse models of type 1 diabetes, highlighting their potential utility for the treatment of human autoimmune disorders.
    Source
    Nat Med. 2013 Dec;19(12):1632-7. doi: 10.1038/nm.3393. Epub 2013 Nov 24. Link to article on publisher's site
    DOI
    10.1038/nm.3393
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/30528
    PubMed ID
    24270545
    Related Resources
    Link to Article in PubMed
    ae974a485f413a2113503eed53cd6c53
    10.1038/nm.3393
    Scopus Count
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