       Document 0564
 DOCN  M9610564
 TI    A functionally compromised intermediate in extrathymic CD8+ T cell
       deletion.
 DT    9601
 AU    Dillon SR; MacKay VL; Fink PJ; University of Washington, School of
       Medicine, Department of; Immunology, Seattle 98195-7650, USA.
 SO    Immunity. 1995 Sep;3(3):321-33. Unique Identifier : AIDSLINE
       MED/96021336
 AB    We have established a model system for analyzing the induction of
       self-tolerance among mature peripheral T cells in V beta 5 TCR Tg mice.
       Both CD4+V beta 5+ and CD8+ V beta 5+ cells undergo a
       superantigen-driven chronic deletion in the periphery of I-E mice. Prior
       to their disappearance, CD4+ transgene-expressing cells are activated
       and then rendered anergic to further stimulation through their TCRs.
       This scenario differs strikingly in the CD8+ cellular compartment, which
       is characterized by a distinct population of CD8loV beta 5lo cells
       localized to the blood and spleen. CD8lo cells are small, express the
       surface phenotype of memory cells, and rapidly incorporate BrdU in vivo.
       The kinetics of their appearance and disappearance in adult
       thymectomized mice, the rapid chasing of BrdU from labeled cells, and
       their in vivo cortisone sensitivity all suggest CD8lo cells are slated
       for deletion. Furthermore, their functional incompetence can be
       documented in vitro in the absence of internucleosomal DNA
       fragmentation. Thus, we have identified an intermediate population of T
       cells targeted for peripheral deletion that, although functionally
       compromised, has not yet undergone programmed cell death.
 DE    Animal  Apoptosis  CD8-Positive T-Lymphocytes/*PHYSIOLOGY  *Immune
       Tolerance  Lymphocyte Transformation  Mice  Mice, Inbred DBA  Mice,
       Transgenic  Receptor-CD3 Complex, Antigen, T-Cell/PHYSIOLOGY  Receptors,
       Antigen, T-Cell, alpha-beta/PHYSIOLOGY  Support, U.S. Gov't, Non-P.H.S.
       Support, U.S. Gov't, P.H.S.  JOURNAL ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).

