We addressed the question of whether the enhanced arthritis development in RP105-/- mice was due to the enhanced response of TLRs to the Mycobacterium-containing adjuvant, CFA, because it has been shown that the in vivo and in vitro response to Mycobacterium tuberculosis is regulated by TLR2, TLR 4, and MyD88 [39-42]. This evidence concerns the gene TLR2 and arthritic joint disease.