SCIRP Mobile Website
Paper Submission

Why Us? >>

  • - Open Access
  • - Peer-reviewed
  • - Rapid publication
  • - Lifetime hosting
  • - Free indexing service
  • - Free promotion service
  • - More citations
  • - Search engine friendly

Free SCIRP Newsletters>>

Add your e-mail address to receive free newsletters from SCIRP.


Contact Us >>

WhatsApp  +86 18163351462(WhatsApp)
Paper Publishing WeChat
Book Publishing WeChat

Article citations


Chang, C. H., S. C. Hong, C. C. Hughes, C. A. Janeway, Jr., and R. A. Flavell. 1995. CIITA activates the expression of MHC class II genes in mouse T cells. Int Immunol 7:1515-1518.

has been cited by the following article:

  • TITLE: Auto-presentation of Staphylococcal enterotoxin A by mouse CD4+ T cells

    AUTHORS: Reuven Rasooly, Paula M. Do, Bradley J. Hernlem

    KEYWORDS: MHC Class II; T-Cell; Enterotoxin

    JOURNAL NAME: Open Journal of Immunology, Vol.1 No.1, June 30, 2011

    ABSTRACT: The currently accepted model for superantigen (SAg) induced T cell activation suggests that SAg, without being processed, cross link both MHC class II, from Antigen Presenting Cells (APC), and V-β , from T-cell receptor (TCR), initi-ating nonspecific T-cell activation. This T-cell proliferation induces a massive cytokine release associated with several human diseases. It is thought that murine CD4+ T cells do not express MHC class-II molecules. However, we discov-ered that a subtype of mouse naïve CD4+ T cells expresses MHC class II on their cell surface and that these CD4+ T cells can perform the role of both APC and T cells, able to present Staphy-lococcal enterotoxin A (SEA) to itself or neigh- boring CD4+ T cells via MHC class II, thus in-ducing massive CD4+ T cell proliferation. Treat- ment with neutralizing anti MHC class II anti-body inhibits this CD4+ T cell proliferation re-sponse. The fact that murine CD4+ T cells ex-press MHC class II offers new insight about SAg activity. Based on our findings, we propose re-vising and extending previous models for SAg induced T cell activation, altering previous models of MHC class II restriction of T cell re-sponses to SEA as well as the requirement for SAg processing.