Document 0111
 DOCN  M9550111
 TI    Costimulatory signals can selectively modulate cytokine production by
       subsets of CD4+ T cells.
 DT    9505
 AU    Shanafelt MC; Soderberg C; Allsup A; Adelman D; Peltz G; Lahesmaa R;
       Department of Leukocyte Biology, Syntex Research, Palo Alto, CA; 94303.
 SO    J Immunol. 1995 Feb 15;154(4):1684-90. Unique Identifier : AIDSLINE
       MED/95138511
 AB    Analysis of experimental animal models and human clinical samples has
       indicated that the selective activation of CD4+ T cell subsets with
       distinct profiles of cytokine production plays an important role in the
       pathogenesis of human inflammatory and allergic diseases. The
       possibility that differential activation of costimulatory pathways is a
       mechanism for selectively modulating cytokine production by CD4+ T cells
       was tested. The proliferative response and cytokines secreted by a panel
       of human CD4+ T cell clones, representative of Th1 or Th2/0 cells, in
       response to activation of different costimulatory pathways was measured.
       CD28-mediated costimulatory signals induced proliferation and IFN-gamma
       secretion by Th1 cells. Although CD28-ligation induced Th2/0 cells to
       proliferate, it did not trigger IL-4 production. Ligation of LFA-1 and
       CD45 isoforms also generated costimulatory signals activating cytokine
       secretion by the different types of T cell clones. Th1 cells secreted
       the same profile of cytokines, irrespective of which costimulatory
       pathway was engaged. However, the cytokine secreted by a subset of Th2/0
       cells varied, depending upon which costimulatory pathways were
       activated. These results suggest that the costimulatory pathways
       activated by APCs can selectively influence cytokine production by CD4+
       T cell subsets.
 DE    Animal  Antigens, CD28/IMMUNOLOGY  Antigens, CD3/IMMUNOLOGY  Cats  Human
       Hypersensitivity, Immediate/BLOOD/IMMUNOLOGY  Interferon Type
       II/BIOSYNTHESIS  Interleukin-4/BIOSYNTHESIS  Lyme
       Disease/BLOOD/IMMUNOLOGY  *Lymphocyte Transformation
       Lymphokines/*BIOSYNTHESIS/SECRETION  Mites  *Signal Transduction
       Support, Non-U.S. Gov't  Th1 Cells/*PHYSIOLOGY  Th2 Cells/*PHYSIOLOGY
       JOURNAL ARTICLE

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