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. Author manuscript; available in PMC: 2010 Oct 1.

Published in final edited form as: Exp Eye Res. 2009 Jun 12;89(4):522–531. doi: 10.1016/j.exer.2009.05.012

Anti-CXCR7 antibody did not mitigate OVA-induced uveitis in DO11.10 mice. DO11.10 mice received a total of 30 μg of polyclonal CXCR7 antibody intraperitoneally over two days (n = 5) or 1.5 μg of CXCR7 antibody intravitreally (n = 3). Twenty four hours after intravitreal OVA challenge, circulating leukocytes were labeled with rhodamine, and ocular inflammatory cells were assessed by intravital microscopy. (A) Representative images of a single frame from intravital microscopy videos taken of the iris at 24 hours during the course of inflammation induced by OVA. Note: CXCR7 antibody did not significantly alter OVA-induced inflammatory cell infiltration in the eye. (B) Quantification of rolling and adherent cells in the vasculature of the iris treated with and without CXCR7 antibody.

Anti-CXCR7 antibody did not mitigate OVA-induced uveitis in DO11.10 mice. DO11.10 mice received a total of 30 μg of polyclonal CXCR7 antibody intraperitoneally over two days (n = 5) or 1.5 μg of CXCR7 antibody intravitreally (n = 3). Twenty four hours after intravitreal OVA challenge, circulating leukocytes were labeled with rhodamine, and ocular inflammatory cells were assessed by intravital microscopy. (A) Representative images of a single frame from intravital microscopy videos taken of the iris at 24 hours during the course of inflammation induced by OVA. Note: CXCR7 antibody did not significantly alter OVA-induced inflammatory cell infiltration in the eye. (B) Quantification of rolling and adherent cells in the vasculature of the iris treated with and without CXCR7 antibody.