Beh?et’s disease (BD) causes a refractory uveoretinitis, with inflammatory cell infiltration including polymorphonucler leukocytes in the eye. Tumor necrosis factor (TNF)-alpha inhibitor, infliximab treatment for BD was well tolerated, with non-serious adverse effects occurring in about half of the patients. At the end of 1 year, uveoretinitis had improved or improved somewhat in 90% over patients, accompanied by improvement in the mean visual acuity. For the proving in this mechanism, we investigated toll like receptor (TLR)2 and TLR4, as receptors of endotoxin expressed on the inflammatory cells, on peripheral blood mononuclear cells (PBMC) of BD patients with uveoretinitis before and after treatment with infliximab. In 23 BD patients with uveoretinitis, the mean frequency of ocular inflammatory attacks per year decreased significantly from 4.1 ± 2.5 before treatment to 0.7 ± 1.0 after treatment with infliximab. In 18 of 23 (78.3%) BD patients treated with infliximab, TLR2 expression on CD14⁺ cells was reduced after treatment compared to before treatment. Mean fluorescence intensity (MFI) of TLR2 expression decreased significantly from 483.8 ± 292.0 before treatment to 337.4 ± 107.0 after treatment. TLR4 expression on CD14⁺ cells was reduced in 20 patients (87.0%).  MFI of TLR4 was decreased significantly (p=0.0275) from 230.0 ± 93.7 before treatment to 177.3 ± 64.0 after treatment.  Intracellular cytokines (IFN-γ, IL-10, IL-17) produced by CD4⁺ T cells were not different before and after treatment. Expressions of TLRs on PBMC were reduced in patients with Beh?et's disease treated with infliximab. In this session, I am going to present TLR expression can be a marker of the efficacy of infliximab treatment in BD patients.