TLR1 and infection: Rather, in genetically susceptible individuals, particularly those with a Toll-like receptor 1 (TLR1) polymorphism [10] and/or certain HLA-DR alleles [11], excessive joint inflammation associated with certain B. burgdorferi strains [6], B. burgdorferi proteins [12] or spirochetal antigens adherent to cartilage surfaces [13], may lead to immune dysregulation of CD4+ T cell subsets [14,15] and infection-induced autoimmunity [16], resulting in persistent joint inflammation after spirochetal killing with antibiotic therapy.