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Kameyama, K., Nemoto, Y., Kanai, T., Shinohara, T., Okamoto, R., Tsuchiya, K., Nakamura, T., Sakamoto, N., Totsuka, T., Hibi, T. and Watanabe, M. (2010) IL-2 Is Positively Involved in the Development of Colitogenic CD4+ IL-7R Alpha High Memory T Cells in Chronic Colitis. European Journal of Immunology, 40, 2423-2436.
http://dx.doi.org/10.1002/eji.200939764
has been cited by the following article:
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TITLE:
Fyn Expression Predicates Both Protective Immunity and Onset of Autoimmunity
AUTHORS:
Behrouz Moemeni, Nathalie Vacaresse, Marina Vainder, Michael E. Wortzman, Tania H. Watts, André Veillette, Thomas F. Gajewski, Michael Julius
KEYWORDS:
Fyn, Lck, TcR Signaling, Immunity, Autoimmunity
JOURNAL NAME:
Open Journal of Immunology,
Vol.5 No.5,
December
3,
2015
ABSTRACT: Genomic disruption of Fyn has not been associated with an immune-deficient phenotype, notwithstanding the profound impairment in IL-2 production by T cells derived from Fyn-deficient animals observed in vitro. The results presented demonstrate that Fyn deficient animals succumb to influenza infection ahead of the protective expansion of lung infiltrating T cells and viral clearance observed in wild-type hosts. Formal proof that Fyn-dependent IL-2 production mediates T cell expansion in vivo is provided using a model of T cell induced enteropathy. Specifically, Fyn deficient naive T cells do not induce colitis in SCID animals due to their lack of expansion, and Fyn re-expression rescues both IL-2 production and its capacity to support in vivo expansion leading to colitis. These results reconcile the obligatory role of Fyn in T cell activation and autocrine IL-2 supported growth; and underscore the mechanism through which its function is integrated with and regulated by Lck.