title: Proliferative response of human CD4+ T lymphocytes stimulated by the lectin jacalin.
abstract: 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.
authors.affiliation: CNRS URA 1172, Immunologie et Interactions Moléculaires, Laboratoire d'Immunologie et Immunopathologie, CHU, Poitiers, France.
authors.forename: E
authors.initials: E
authors.lastname: Blasco
authors.forename: A
authors.initials: A
authors.lastname: Barra
authors.forename: M
authors.initials: M
authors.lastname: Nicolas
authors.forename: J C
authors.initials: JC
authors.lastname: Lecron
authors.forename: J
authors.initials: J
authors.lastname: Wijdenes
authors.forename: J L
authors.initials: JL
authors.lastname: Preud'homme
mesh_terms: D015703:Antigens, CD / Q000378:metabolism; D001667:Binding, Competitive; D015704:CD4 Antigens / Q000502:physiology; D015496:CD4-Positive T-Lymphocytes / Q000187:drug effects* / Q000276:immunology; D018956:CD5 Antigens; D016207:Cytokines / Q000096:biosynthesis; D005677:G(M1) Ganglioside / Q000378:metabolism; D015870:Gene Expression / Q000187:drug effects; D006801:Humans; D016130:Immunophenotyping; D066298:In Vitro Techniques; D007376:Interleukin-2 / Q000096:biosynthesis / Q000235:genetics; D037102:Lectins / Q000494:pharmacology*; D008213:Lymphocyte Activation / Q000187:drug effects*; D008553:Melibiose / Q000494:pharmacology; D008756:Methylgalactosides / Q000494:pharmacology; D009000:Monocytes / Q000276:immunology; D037121:Plant Lectins; D012333:RNA, Messenger / Q000235:genetics
chemical_list: D015703:Antigens, CD; D015704:CD4 Antigens; D018956:CD5 Antigens; D016207:Cytokines; D007376:Interleukin-2; D037102:Lectins; D008756:Methylgalactosides; D037121:Plant Lectins; D012333:RNA, Messenger; C043696:jacalin; D005677:G(M1) Ganglioside; D008553:Melibiose