CX3CR1 and hemolytic-uremic syndrome: Based on this evidence, we can speculate that in γδ T cells, CX3CR1 could play a role by recruiting them to the glomeruli initially affected by the Stx2a and then to promote the γδ T cell participation in the inflammation process, thus contributing to the exacerbation of the endothelial damage and in the pathogenesis of HUS.