Group B Streptococcus Induces a Robust IFN-γ Response by CD4+ T Cells in an In Vitro d In Vivo Model

Group B Streptococcus (GBS) sero type Ill causes life-threatening infections. Cytokines have emerged as important players for the control of disease, particularly IFN-gamma. Although potential sources of this cytokine have been proposed, no specific cell line has ever been described as a leading contributor. In this study, (De 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-gamma, TNF-alpha, and IL-6 and actively recruit T cells via chemokines like CXCL9, CXCL10, and CCL3. Responding CDT' T cells differentiate into cells producing large amounts of IFN-gamma, TNF-alpha, and IL-2. In vitro studies using dendritic cell and CDT+ 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 ITN-gamma, production. Overall, CD4(+) T cells are important producers of IFN-gamma and might thus influence the course of GBS infection through the expression balance of this cytokine.