In in vitro infection models after an initial activation of gene expression, MAP rapidly (within 6-24 h) shuts down the pro-inflammatory T cell immunity by induction of immunosuppressive cytokines (IL-10, TGF-β), impairment of CD40 signaling which is an important macrophage receptor for CD40L on Th1 type T cells to maintain a Th1 immune response [66]. Here, IL10 is linked to infection.