Superoxide dismutase 3 attenuates experimental Th2-driven allergic conjunctivitis

- Clinical signs associated with conjunctivitis are reduced in mice treated with SOD3.
- SOD3 inhibits DC maturation and Th cell infiltration in conjunctiva of EAC.
- Characteristics of EAC are correlated with the absence of SOD3.
- SOD3 is necessary for prevention of Th2-driven allergic conjunctival inflammation.

Allergic conjunctivitis is an inflammatory eye disease mediated by Th2 type immune response. The role of extracellular superoxide dismutase 3 (SOD3) in immune response and allergic conjunctival inflammation was examined in a murine model for experimental allergic conjunctivitis (EAC). Allergic conjunctivitis was induced in mice by allergen challenge with ovalbumin in alum via the conjunctival sac. SOD3 was topically applied and allergy indicators were compared. Clinical signs associated with conjunctivitis, such as OVA-specific IgE production, IgG1/G2a ratio and eosinophil infiltration, were drastically reduced in mice treated with SOD3. They also had less dendritic cells and CD4+ T cells in conjunctiva than controls. Attenuated allergic inflammation was accredited to reduced Th2 type cytokine responses and increased Treg cytokine in draining lymph node. The characteristics of EAC were attributed to the absence of SOD3. Our findings suggest that SOD3 might be considered as a potential target for Th2-driven allergic conjunctival inflammation.