Document 0136
 DOCN  M95B0136
 TI    Proliferative response of human CD4+ T lymphocytes stimulated by the
       lectin jacalin.
 DT    9511
 AU    Blasco E; Barra A; Nicolas M; Lecron JC; Wijdenes J; Preud'homme JL;
       CNRS URA 1172, Immunologie et Interactions Moleculaires,; Laboratoire
       d'Immunologie et Immunopathologie, CHU, Poitiers,; France.
 SO    Eur J Immunol. 1995 Jul;25(7):2010-8. Unique Identifier : AIDSLINE
       MED/95347403
 AB    The Gal beta(1-3)GalNAc-binding lectin jacalin is known to specifically
       induce the proliferation of human CD4+ T lymphocytes in the presence of
       autologous monocytes and to interact with the CD4 molecule and block
       HIV-1 infection of CD4+ cells. We further show that jacalin-induced
       proliferation is characterized by an unusual pattern of T cell
       activation and cytokine production by human peripheral blood mononuclear
       cells (PBMC). A cognate interaction between T cells and monocytes was
       critical for jacalin-induced proliferation, and human recombinant
       interleukin (IL)-1 and IL-6 did not replace the co-stimulatory activity
       of monocytes. Blocking studies using monoclonal antibodies (mAb) point
       out the possible importance of two molecular pathways of interaction,
       the CD2/LFA-3 and LFA-1/ICAM-1 pathways. One out of two anti-CD4 mAb
       abolished jacalin responsiveness. Jacalin induced interferon-gamma and
       high IL-6 secretion, mostly by monocytes, and no detectable IL-2
       synthesis or secretion by PBMC. In contrast, jacalin-stimulated Jurkat T
       cells secreted IL-2. CD3- Jurkat cell variants failed to secrete IL-2,
       suggesting the involvement of the T cell receptor/CD3 complex pathway in
       jacalin signaling. IL-2 secretion by CD4- Jurkat variant cells was
       delayed and lowered. In addition to CD4, jacalin interacts with the CD5
       molecule. Jacalin-CD4 interaction and the proliferation of PBMC, as well
       as IL-2 secretion by Jurkat cells were inhibited by specific
       jacalin-competitive sugars.
 DE    Antigens, CD/METABOLISM  Antigens, CD4/PHYSIOLOGY  Binding, Competitive
       Cytokines/BIOSYNTHESIS  CD4-Positive T-Lymphocytes/*DRUG
       EFFECTS/IMMUNOLOGY  G(M1) Ganglioside/METABOLISM  Gene Expression/DRUG
       EFFECTS  Human  Immunophenotyping  In Vitro
       Interleukin-2/BIOSYNTHESIS/GENETICS  Lectins/*PHARMACOLOGY  Lymphocyte
       Transformation/*DRUG EFFECTS  Melibiose/PHARMACOLOGY
       Methylgalactosides/PHARMACOLOGY  Monocytes/IMMUNOLOGY  RNA,
       Messenger/GENETICS  Support, Non-U.S. Gov't  JOURNAL ARTICLE

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