Enhancement by vasoactive intestinal peptide of gamma-interferon production by antigen-stimulated type 1 helper T cells.

• Main Authors: Jabrane-Ferrat, N., Bloom, D., Wu, A., Li, L., Lo, D., Sreedharan, S. P., Turck, C. W., Goetzl, A. E.
• Other Authors: Department of Medicine, Microbiology and Immunology (UCSF-HHMI), University of California San Francisco (UC San Francisco), University of California (UC)-University of California (UC)-Rosalind Russell Medical Research Center, Center for Research in Ceramic and Composite Materials (CICECO), Universidade de Aveiro, Institut de Chimie et Biochimie Moléculaires et Supramoléculaires (ICBMS), Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-École Supérieure de Chimie Physique Électronique de Lyon (CPE)-Institut National des Sciences Appliquées de Lyon (INSA Lyon), Université de Lyon-Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Institut de Chimie - CNRS Chimie (INC-CNRS)-Centre National de la Recherche Scientifique (CNRS)
• Format: Article in Journal/Newspaper
• Language: English
• Published: HAL CCSD 1999
• Subjects: MESH: Animals; MESH: Antigen Presentation; MESH: Vasoactive Intestinal Peptide; MESH: Antigens; MESH: Female; MESH: Interferon-gamma; MESH: Lymphocyte Activation; MESH: Mice; Inbred BALB C; MESH: Receptors; Vasoactive Intestinal Peptide; MESH: Th1 Cells; [SDV.CAN]Life Sciences [q-bio]/Cancer; Sperm whale
• Online Access: https://hal.science/hal-00641045

International audience Vasoactive intestinal peptide (VIP) is a neuroendocrine mediator in immune tissues that affects many T cell functions through two homologous high-affinity G-protein-coupled receptors, termed VIPR1 and VIPR2. Antigen-stimulated secretion of gamma-interferon (IFN-gamma) by sperm whale myoglobin-specific Th1 cells of DBA/2 mouse I-Ed-restricted clones, which express VIPR1 and VIPR2, was enhanced by 10(-10) M to 10(-7) M VIP. Enhancement of IFN-gamma secretion reached a mean maximum of fourfold for VIP and threefold for a VIPR2-selective agonist, without any effect of a VIPR1-selective agonist. Secretion of IFN-gamma by PMA and ionomycin-stimulated clones of Th1 cells was not altered by VIP. Antigen-stimulated secretion of IFN-gamma by T cell receptor-transgenic, influenza hemagglutinin-specific, and cytokine-differentiated mouse lymph node Th1 cells, which also express VIPR1 and VIPR2, was enhanced by 10(-10) M to 10(-8) M VIP. Enhancement of IFN-gamma secretion increased to a maximum of 14-fold for VIP, 14-fold for the VIPR2-selective agonist, and 20-fold for the VIPR1-selective agonist. In contrast to VIP suppression of interleukin production and lack of effect on IFN-gamma production by T cells stimulated with anti-CD3 antibody or a mitogenic lectin, generation of IFN-gamma by antigen-stimulated T cells is enhanced significantly by physiological concentrations of VIP.