Activated human B cells stimulate COX-2 expression in follicular dendritic cell-like cells via TNF-α. (February 2018)

• Record Type: Journal Article
• Authors: Kim, Jini; Lee, Seungkoo; Jeoung, Dooil; Kim, Young-Myeong; Choe, Jongseon
• Is Part Of: Molecular immunology. Volume 94(2018:Feb.)
• Page Start: 1
• Page End: 6
• Publication Date: 2018-02
• Subjects: COX cyclooxygenase -- FDC follicular dendritic cell -- GC germinal center -- LPS lipopolysaccharide -- PG prostaglandin -- PGIS prostaglandin I synthase -- TD thymus-dependent; Follicular dendritic cell -- COX-2 -- B cell -- TNF-α; Immunochemistry -- Periodicals; Molecular biology -- Periodicals; Immunochemistry -- Periodicals; Allergy and Immunology -- Periodicals; Molecular Biology -- Periodicals; Immunochimie -- Périodiques; Biologie moléculaire -- Périodiques; Immunochemistry; Molecular biology; Periodicals; Electronic journals; 571.96
• DOI: 10.1016/j.molimm.2017.12.004
• Languages: English
• ISSNs: 0161-5890

Abstract

Highlights: Activated human B cells stimulate COX-2 expression in FDC-like cells. FDCs but not B cells express COX-2 in the germinal center. TNF-α mediates the B-cell-induced COX-2 expression. Abstract: In spite of the potential importance of cyclooxygenase (COX)-2 expression in the germinal center, its underlying cellular and molecular mechanisms are largely unknown. COX-2 is the key enzyme generating pleiotropic prostaglandins. Based on our previous findings, we hypothesized that lymphocytes would stimulate COX-2 expression in follicular dendritic cell (FDC) by liberating cytokines. In this study, we examined the effect of tonsillar lymphocytes on COX-2 expression in FDC-like cells by immunoblotting. B but not T cells induced COX-2 protein in a time- and dose-dependent manner. Sub-fractionation analysis of B cell subsets revealed that activated but not resting B cells were responsible for the COX-2 induction. Confocal microscopy of frozen tonsils demonstrated that FDCs indeed express COX-2 in situ, in line with the in vitro results. To identify the stimulating molecule, we added neutralizing antibodies to the coculture of FDC-like cells and B cells. COX-2 induction in FDC-like cells was markedly inhibited by TNF-α neutralizing antibody. Finally, the actual production of TNF-α by activated B cells was confirmed by an enzyme immunoassay. The current study implies an unrecognized cellular interaction between FDC and B cells leading to COX-2 expression during immune inflammatory responses.