We have demonstrated a higher expression of TLR4 on uvea-resident tissue macrophages in endotoxin-induced acute anterior uveitis than is found in normal rats and we have proposed a pathogenic mechanism whereby LPS of Gram-negative bacteria (GNB) could initiate uveitis by activation of intraocular TLR4 and produce proinflammatory cytokines and chemokines for the recruitment of leukocytes to the eye [6]. Here, TLR4 is linked to anterior uveitis.