Figure 1.

GBS transition to invasive disease. GBS lipoproteins, GAPDH, and nucleic acids majorly contribute to intestinal immune activation inducing pro-inflammatory responses, neutrophil recruitment, cellular proliferation, maturation and, finally, microbial clearance. Early induction of specific antibody release by B plasma cells and IL-10 secretion by both B-lymphocytes and phagocytes act as a negative feedback loop to counter-regulate hyperinflammation. Uncontrolled increase of IL-10, in contrast, hampers neutrophil recruitment and bacterial elimination. At the same time, T-lymphocytes can directly interact with GBS ligands or receive pro-inflammatory signals via monocytic cytokines. While Th1 and Th17 cells promote infection control, activation of regulatory T cells prevents hyperinflammation and supports post-infectious healing.