However, the contribution of TLR signalling to this phenomenon is still a mater of discussion; Scumpia et al[31] described that this expansion following bacterial infection occurs in the absence of TLR signalling, whereas Singh et al[7] found that the LKS expansion after vaccinia virus infection is dependent on MyD88, and in this work we have found that the expansion is delayed in the absence of TLR2 signalling during candidiasis. The gene discussed is TLR2; the disease is bacterial infectious disease.