44
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      Mouse CD1-specific NK1 T cells: development, specificity, and function.

      1 , , ,
      Annual review of immunology
      Annual Reviews

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          NK1 T cells are a specialized population of alpha/beta T cells that coexpress receptors of the NK lineage and have the unique potential to very rapidly secrete large amounts of cytokines, providing early help for effector cells and regulating the Th1 or Th2 differentiation of some immune responses. NK1 T cells express a restricted TCR repertoire made of an invariant TCR alpha chain, V alpha 14-J alpha 281, associated with polyclonal V beta 8, V beta 7, and V beta 2 TCR beta chains. NK1 T cells recognize the products of the conserved family of MHC class I-like CD1 genes, apparently in the absence of foreign antigens. Thus, this novel regulatory pathway, which straddles the innate and the adaptive immune systems, is unique in that its activation may not require associative recognition of antigen. Here, we review the specificity and function of mouse NK1 T cells, and we discuss the relationship of this lineage to mainstream T cells and NK cells.

          Related collections

          Author and article information

          Journal
          Annu Rev Immunol
          Annual review of immunology
          Annual Reviews
          0732-0582
          0732-0582
          1997
          : 15
          Affiliations
          [1 ] Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544, USA. abendelac@molbiol.princeton.edu
          Article
          10.1146/annurev.immunol.15.1.535
          9143699
          5b3703dc-43dd-40e7-8124-dfdeffd9999e
          History

          Comments

          Comment on this article