Group B Streptococcus Induces a Robust IFN-γ Response by CD4+ T Cells in an In Vitro and In Vivo Model. (16th February 2016)

• Record Type: Journal Article
• Authors: Clarke, Damian; Letendre, Corinne; Lecours, Marie-Pier; Lemire, Paul; Galbas, Tristan; Thibodeau, Jacques; Segura, Mariela
• Other Names: Rosa Daniela Academic Editor.
• Is Part Of: Journal of immunology research. Volume 2016(2016)
• Publication Date: 2016-02-16
• Subjects: Immunology -- Periodicals; Immunology -- Research -- Periodicals; 616.07905
• DOI: 10.1155/2016/5290604
• Languages: English
• ISSNs: 2314-8861

Abstract

Abstract : Group B Streptococcus (GBS) serotype III causes life-threatening infections. Cytokines have emerged as important players for the control of disease, particularly IFN- γ . Although potential sources of this cytokine have been proposed, no specific cell line has ever been described as a leading contributor. In this study, CD4 + T cell activation profiles in response to GBS were evaluated through in vivo, ex vivo, and in vitro approaches. Total splenocytes readily produce a type 1 proinflammatory response by releasing IFN- γ, TNF- α, and IL-6 and actively recruit T cells via chemokines like CXCL9, CXCL10, and CCL3. Responding CD4 + T cells differentiate into Th1 cells producing large amounts of IFN- γ, TNF- α, and IL-2. In vitro studies using dendritic cell and CD4 + T cell cocultures infected with wild-type GBS or a nonencapsulated mutant suggested that GBS capsular polysaccharide, one of the major bacterial virulence factors, differentially modulates surface expression of CD69 and IFN- γ production. Overall, CD4 + T cells are important producers of IFN- γ and might thus influence the course of GBS infection through the expression balance of this cytokine.