Given the drastic shifts in Treg-associated expression of CTLA-4 and GITR that each correlates with the reduced suppressive potency of these cells from early to late time points during persistent Salmonella infection, additional experiments sought to identify the relative importance of these molecules in dictating infection tempo using well characterized CTLA-4 blocking (clone UC10-4F10) or GITR-stimulating (clone DTA-1) monoclonal antibodies [54], [62], [63], [64]. This evidence concerns the gene TNFRSF18 and infection.