Concanavalin A-mediated T cell proliferation is regulated by herpes virus entry mediator costimulatory molecule

• Published in: In vitro cellular & developmental biology. Animal 2014-04, Vol.50 (4), p.313-320
• Main Authors: Ando, Yoshiaki, Yasuoka, Chika, Mishima, Takuya, Ikematsu, Takuya, Uede, Toshimitsu, Matsunaga, Tsukasa, Inobe, Manabu
• Format: Article
• Language: English
• Subjects: Animal Genetics and Genomics; Biomedical and Life Sciences; CD28 Antigens - immunology; CD28 Antigens - metabolism; Cell Biology; Cell Culture; Cell growth; CELL GROWTH/DIFFERENTIATION/APOPTOSIS; cell proliferation; Cell Proliferation - drug effects; concanavalin A; Concanavalin A - administration & dosage; Concanavalin A - immunology; Developmental Biology; Gene expression regulation; Herpesviridae; Herpesvirus; Herpesvirus 1, Cercopithecine - immunology; Herpesvirus 1, Cercopithecine - metabolism; Humans; Immunoglobulin Fc Fragments - immunology; Immunoglobulin Fc Fragments - metabolism; immunoglobulin G; Immunoglobulin G - immunology; Immunoglobulin G - metabolism; Life Sciences; Ligands; Lymphocyte Activation - immunology; Mice; Mitogens; Molecules; Receptors; Receptors, Tumor Necrosis Factor, Member 14 - immunology; Receptors, Tumor Necrosis Factor, Member 14 - metabolism; recombinant proteins; Signal Transduction - drug effects; Stem Cells; T lymphocytes; T-Lymphocytes - drug effects; T-Lymphocytes - immunology; T-Lymphocytes - metabolism; Viruses
• ISSN: 1071-2690; 1543-706X
• DOI: 10.1007/s11626-013-9705-2

T cell activation is regulated by two distinct signals, signals one and two. Concanavalin A (ConA) is an antigen-independent mitogen and functions as signal one inducer, leading T cells to polyclonal proliferation. CD28 is known to be one of major costimulatory receptors and to provide signal two in the ConA-induced T cell proliferation. Here, we have studied the implication of other costimulatory pathways in the ConA-mediated T cell proliferation by using soluble recombinant proteins consisting of an extracellular domain of costimulatory receptors and Fc portion of human IgG. We found that T cell proliferation induced by ConA, but not PMA plus ionomycin or anti-CD3 mAb, is significantly inhibited by herpes virus entry mediator (HVEM)-Ig, even in the presence of CD28 signaling. Moreover, the high concentration of HVEM-Ig molecules almost completely suppressed ConA-mediated T cell proliferation. These results suggest that HVEM might play more important roles than CD28 in ConA-mediated T cell proliferation.