Human follicular dendritic cells promote the APC capability of B cells by enhancing CD86 expression levels

• Published in: Cellular immunology 2012, Vol.273 (2), p.109-114
• Main Authors: Kim, Jini, Kim, Young-Myeong, Jeoung, Doo-Il, Choe, Jongseon
• Format: Article
• Language: English
• Subjects: Antigen Presentation; B cells; B-Lymphocytes - cytology; B-Lymphocytes - drug effects; B-Lymphocytes - immunology; B7-2 Antigen - antagonists & inhibitors; B7-2 Antigen - genetics; B7-2 Antigen - immunology; B7-2 Antigen - metabolism; Cell Adhesion - immunology; Cell Communication - genetics; Cell Communication - immunology; Co-stimulation; Coculture Techniques; Cytochrome P-450 Enzyme System - immunology; Cytochrome P-450 Enzyme System - metabolism; Dendritic Cells, Follicular - cytology; Dendritic Cells, Follicular - drug effects; Dendritic Cells, Follicular - immunology; Epoprostenol - immunology; Epoprostenol - metabolism; Flow Cytometry; Gene Expression; Human; Humans; Immunity, Innate; Indomethacin - pharmacology; Intramolecular Oxidoreductases - immunology; Intramolecular Oxidoreductases - metabolism; Lipid mediators; Lymphocyte Activation; Palatine Tonsil - cytology; Palatine Tonsil - immunology; Primary Cell Culture; Prostaglandin Antagonists - pharmacology; Receptors, Prostaglandin E, EP4 Subtype - antagonists & inhibitors; Receptors, Prostaglandin E, EP4 Subtype - immunology; Stromal cells; T-Lymphocytes - cytology; T-Lymphocytes - drug effects; T-Lymphocytes - immunology
• ISSN: 0008-8749; 1090-2163
• DOI: 10.1016/j.cellimm.2012.01.003

► FDCs enhance CD86 of B cell. ► Enhanced antigen-presenting ability by FDC-cocultured B cells. ► That is inhibited by anti-CD86 neutralizing antibody. Follicular dendritic cells (FDCs) are an essential cellular component of the germinal center (GC) and are believed to exert regulatory effects on the various stages of GC reactions. According to our previous reports, human FDCs express prostacyclin synthase, and prostacyclin analogues augment adhesion and co-stimulatory molecules on the surface of activated B cells. These findings prompted us to investigate whether FDCs would contribute to the antigen-presenting capability of B cells by using the well-established FDC-like cells, HK cells, and tonsillar B cells. Our results show that HK cells significantly enhance the expression levels of CD54, CD80, and CD86 on the surface of activated B cells. The enhancing effect of HK cells on CD86 is impeded by indomethacin and an EP4 antagonist, implying that a certain prostaglandin is mediating the up-regulation. Prostacyclin indeed recapitulates the enhancing effect on CD86, which is inhibited by EP4 as well as IP antagonists. B cells co-cultured with HK cells exhibit an augmented APC activity, which is inhibited by CD86 neutralization. These results reveal another unrecognized function of human FDC.