SOCS3 and infection: Ablation of SOCS3 within myeloid cells resulted in enhanced IL-6 signaling which inhibited the secretion of TNF-α and IL-12 required to mediate the development of a robust CD4+ T cell response against the infection (221), as well as increased production of NOS2 and Arg1, leading to higher bacterial loads and exacerbated pulmonary inflammation (210).