OX40 agonism also transiently increased the fraction of parenchymal CD4 T cells, and significantly shifted CD4 T cell phenotypes towards those expressing FOXP3 and away from terminal differentiation (CX3CR1, KLRG1), suggesting that the lack of adverse effects may be due to expansion of both effector and regulatory cell populations which can maintain inflammatory balance during infection. This evidence concerns the gene KLRG1 and infection.