MYD88 and infection: The latest study performed to describe the method of action of lipoxin- and L-kynurenine-induced SOCS2 in the pro-inflammatory response during infection also with T. gondii showed the engagement of both mediators in the inhibition of TLR/MyD88, TLR/TRIF, IL-1R/MyD88, and CD40/CD154 signaling pathways [16] (Fig. 1).