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Theoretical model for the modulatory role of Slit2 on intra-orbital pathogenesis of TAO. When CD34− OF-derived Slit2 predominates, the inflammatory phenotype of CD34+ OF is down regulated and the patient with GD either fails to manifest TAO or the disease is mild (Left panel). When CD34+ OF dominates the fibroblast population and the impact of Slit2 is inadequate, TAO is severe (Right panel).
