By Ellen Heber - Katz , : I : Ronald

نویسندگان

  • ELLEN HEBER-KATZ
  • RONALD H. SCHWARTZ
  • LOUIS A. MATIS
  • CHARLES HANNUM
  • THOMAS FAIRWELL
  • ETTORE APPELLA
  • DANIEL HANSBURG
چکیده

It is generally believed (1-3) that T lymphocytes recognize antigen in association with products of the major histocompatibility complex (MHC).I If we consider T cell responsiveness in terms of a recognition unit, it would be made up of three components: antigen, a T cell receptor (s), and a surface Ia molecule on an antigenpresenting cell (APC). In such a model, lack of responsiveness (Ir gene defects) could be explained by a defect of either antigen-Ia, antigen-receptor, or Ia-receptor interaction, or any combination of these. An understanding of these MHC-associated Ir gene defects as well as the mechanism of antigen-induced T cell activation requires the ability to examine the contribution of each component separately by holding the other two components constant. We encountered a unique opportunity to explore this issue using T cell clones specific for cytochrome c. In investigating the T cell responses of B10.A and B10.A(5R) mice to a family of cytochrome c peptides, it was found that these two strains, differing only in the K region, and I-A and L B subregions of the MHC, each had a characteristic pattern of responsiveness to a given set of cytochrome c cyanogen bromide cleavage fragments (4-6). When T cell clones were derived from either of these cytochrome c-immune animals and tested for antigen specificity, the response profiles of the clones closely resembled those of the whole lymph node population. Remarkably, however, the clones from either strain responded to antigen on both B10.Aand B10.A(5R)presenting cells. Furthermore, the response pattern of either set of clones resembled that of the whole B10.A lymph node population when B10.A-presenting cells were

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تاریخ انتشار 2003