Figure 1.

Blocking OX40 signaling by anti-OX40L antibody attenuates OVA-induced uveitis. OVA was administered intravitreally into the DO11.10 mice, which have transgenic dsRed fluorescent protein under the control of CD4 promoter. In addition, some mice were simultaneously treated with anti-OX40L antibody during intravitreal OVA challenge. Ocular-infiltrating cells were assessed by intravital microscopy at 48 hours. Representative image of a single frame from intravital microscopy videos taken of the iris during the course of inflammation induced by OVA (n = 3 mice per group). Of note, intravitreal OVA challenge elicited a marked infiltration of red fluorescent T cells in the extravascular area of the iris (A), which was substantially inhibited by anti-OX40L antibody (B). In addition, intravascular leukocytes of regular DO11.10 mice were labeled with rhodamine at 48 hours after intravitreal OVA stimulation, and ocular inflammatory cells were assessed by intravital microscopy. Of note, compared to OVA challenge alone (C), anti-OX40L antibody inhibited OVA-induced inflammatory cell infiltration in the eye (D). E: Quantitation of rolling and adherent cells in the vasculature of the iris treated with and without anti-OX40L antibody. *P < 0.05.