Naturally occurring Toll-like receptor 11 (TLR11) and Toll-like receptor 12 (TLR12) polymorphisms are not associated with Toxoplasma gondii infection in wild wood mice

Toxoplasma gondii is a highly successful parasite with a worldwide prevalence. Small rodents are the mainintermediate hosts, and there is growing evidence that T. gondii modifies their behaviour. Chronicallyinfected rodents show impaired learning capacity, enhanced activity, and, most importantly, a reductionof the innate fear towards cat odour. This modification of host behaviour ensures a successful transmissionof T. gondii from rodents to felids, the definitive hosts of the parasite. Given the negative fitness consequencesof this behavioural manipulation, as well as an increased mortality during the acute phase ofinfection, we expect rodents to evolve potent resistance mechanisms that prevent or control infection.Indeed, studies in laboratory mice have identified candidate genes for T. gondii resistance. Of particularimportance appear to be the innate immune receptors Toll-like receptor 11 (TLR11) and Toll-like receptor12 (TLR12), which recognise T. gondii profilin and initiate immune responses against the parasite.Here we analyse the genetic diversity of TLR11 and TLR12 in a natural population of wood mice (Apodemussylvaticus), and test for associations between TLR11 and TLR12 polymorphisms and T. gondii infection, aswell as for epistatic interactions between TLR11 and TLR12 on infection status. We found that both TLR11and TLR12 were polymorphic in wood mice, with four and nine amino acid haplotypes, respectively. However,we found no evidence that TLR11 or TLR12 genotypes or haplotypes were significantly associated withToxoplasma infection. Despite the importance of TLR11 and TLR12 in T. gondii recognition and immunedefence initiation, naturally occurring polymorphisms at TLR11 and TLR12 thus appear to play a minor rolein mediating qualitative resistance to T. gondii in natural host populations of A. sylvaticus. This highlights theimportance of assessing the role of candidate genes for parasite resistance identified in a laboratory settingin an ecologically meaningful context to quantify their role in mediating host–parasite interactions in thewild