Consequently, it is currently unclear whether the dysregulated IL-12 pathway in WSX-1−/− mice during infection, and the corresponding development of KLRG-1+ Th1 cells, is due to intrinsic loss of WSX-1 mediated regulation within the innate system, specifically by macrophages and dendritic cells, or whether it is a consequence of abrogated WSX-1 expression on CD4+ T cells, which subsequently leads to amplification of the innate immune response, initiating a positive inflammatory feedback loop. This evidence concerns the gene KLRG1 and infection.