Group BStreptococcusInduces a Robust IFN-γResponse by CD4+T Cells in anIn VitroandIn VivoModel
Group BStreptococcus(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 throughin vivo,ex vivo,andin vitroapproaches. 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 vitrostudies 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-γproduction. Overall, CD4+T cells are important producers of IFN-γand might thus influence the course of GBS infection through the expression balance of this cytokine.