Innate memory phenotype CD4+ T cells play a role in early protection against infection by Listeria monocytogenes in a CD30L-dependent manner.

CD30 ligand (CD30L, CD153) is a type II membrane-associated glycoprotein belonging to the tumor necrosis factor family. It is shown here that CD30L knock out (KO) mice are highly susceptible to primary infection with Listeria monocytogenes as assessed by the survival rate. There were significantly more bacteria on day 3 after infection in the peritoneal cavity, spleen and liver of CD30LKO mice than in wild type (WT) mice. The innate function of memory phenotype (MP) CD44+ CD4+ T cells for interferon-gamma production was significantly lower in CD30LKO mice than in WT mice in response to interleukin (IL)-12 and IL-15 in vitro. Depletion of CD4+ T cells by in vivo administration of anti-CD4 mAb at an early stage after infection hampered protection against Listeria. Furthermore, in vivo administration of agonistic anti-CD30 mAb restored protection against Listeria in CD30LKO mice, whereas treatment with soluble mCD30-Ig hampered protection in WT mice. Taken together, it appears that CD30L/CD30 signaling plays an important role in innate MPCD4+ T cell-mediated protection against infection with L. monocytogenes.