A penetrating ocular injury can affect the induction of anterior chamber-associated immune deviation

To determine the effect of penetrating ocular injury on the induction of anterior chamber-associated immune deviation (ACAID).

An injection of 5 mul ovalbumin (OVA, 20 mg/ml) into the anterior chamber (AC) of female BALB/c mice was performed to induce ACAID. A penetrating ocular injury was induced via the limbus on OVA-inoculated eyes at 24 h, 48 h, 72 h, and 120 h following AC injection. The mice receiving an OVA inoculation without the ocular injury served as the AC-injection group. Delayed type hypersensitivity (DTH) was examined to evaluate the induction of ACAID. The levels of transforming growth factor (TGF)-beta1, interleukin (IL)-10, and interferon (IFN)-gamma produced by splenocytes were detected by enzyme-linked immunosorbent assays (ELISA). The frequency of CD4(+)CD25(+)Foxp3(+)T cells in the splenocytes was detected by flow cytometry.

A significantly decreased DTH response was observed in the AC-injection group as well as in mice that received a penetrating injury at 72 h and 120 h following AC-injection of OVA. The levels of TGF-beta1 and IL-10 produced by splenocytes of mice in the AC-injection group and in the 72-h and 120-h group were significant higher than those in the 24-h and 48-h group. However, the levels of IFN-gamma produced by splenocytes of the AC-injection group and the 72-h and 120-h group were significantly lower than those in the 24-h and 48-h group. An increased frequency of CD4(+)CD25(+)Foxp3(+)T cells was found in the AC-injection group and the 72-h and 120-h group.

Penetrating ocular injury preformed shortly (24 h-48 h) after an AC injection of an antigen was able to abrogate ACAID and was associated with a decreased production of TGF-beta1 and IL-10, an increased production of IFN-gamma, and a decreased expression of CD4(+)CD25(+)Foxp3(+)T cells.