       Document 0997
 DOCN  M9540997
 TI    Differential ability of Th1 and Th2 T cells to express Fas ligand and to
       undergo activation-induced cell death.
 DT    9504
 AU    Ramsdell F; Seaman MS; Miller RE; Picha KS; Kennedy MK; Lynch DH;
       Department of Immunobiology, Immunex Research and Development;
       Corporation, Seattle, WA.
 SO    Int Immunol. 1994 Oct;6(10):1545-53. Unique Identifier : AIDSLINE
       MED/95127557
 AB    Stimulation of previously activated T cells through the antigen receptor
       can result in the apoptotic death of the responding cell, a process
       referred to as activation-induced cell death (AICD). This process
       appears to involve Fas (CD95) and its ligand (Fas-L). The distribution
       of Fas and Fas-L on various T cell subsets has not been extensively
       characterized. We have therefore analyzed cells committed to a Th1- or
       Th2-type differentiation pattern for the expression and function of
       Fas-L. Using both a sensitive bioassay and flow cytometry, we
       demonstrate that cloned Th1 cells express high levels of Fas-L, whereas
       cloned Th2 cells express only low levels. The expression of Fas-L by Th1
       and Th2 cells correlates with the relative abilities of these two cell
       types to undergo AICD. Whereas AICD is readily observed in cultures of
       cloned Th1, but not Th2 cells, Th2 cells are capable of undergoing
       apoptosis in the presence of Th1 cells expressing Fas-L. The ability of
       T cells to undergo AICD appears to be unrelated to the presence of
       various cytokines. Thus, the Fas/Fas-L pathway appears to be critical
       for the induction of AICD and this pathway is differentially regulated
       in cells committed to either Th1 or Th2 differentiation.
 DE    Animal  Antigens, Surface/*BIOSYNTHESIS  Apoptosis/*IMMUNOLOGY  Clone
       Cells  Comparative Study  Cytotoxicity Tests, Immunologic  Flow
       Cytometry  Human  Membrane Glycoproteins/*BIOSYNTHESIS  Receptors,
       Antigen, T-Cell, alpha-beta/IMMUNOLOGY  Th1 Cells/*IMMUNOLOGY  Th2
       Cells/*IMMUNOLOGY  JOURNAL ARTICLE

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

