In support of this concept, exogenous IFN-γ has been shown to reduce Tfh and GC B cell responses to Plasmodium yoelii (102), and the blockade of CXCR3-mediated signals was found to enhance precursor Tfh cell accumulation in the spleen of malaria-infected mice, thereby favoring parasitic clearance (115). This evidence concerns the gene IFNG and malaria.