Abstract
Purpose: :
We have shown previously that an intracameral injection of antigen results in CCR2/CCL2- driven infiltration of circulating monocytes into the anterior chamber (AC).We therefore investigated further the phenotype of these recruited monocytes and their role in the induction of anterior chamber-associated immune deviation (ACAID).
Methods: :
Irides from mice receiving an intracameral injection of ovalbumin (OVA) were recovered and digested with collagenase/dispase to prepare cell suspensions that were stained with antibodies for inflammatory monocytes. and analyzed by flow cytometry. The effect of the indazolic derivative bindarit on the production of CCL2 in aqueous humor was determined by the intracamaeral, intravitreous or intraperitoneal injection of bindarit prior to the intracameral injection of OVA.
Results: :
Monocytes recruited to the iris post intracameral injection were CD45+, F4/80 lo, CD11b hi,GR1hi, Ly6c hi, Ly6B [7/4+], CD62L+, CD49B+, CD115+. There was an 85% reduction in the infiltration of these monocytes to the iris in CCR2null or CCL2null mice. CD45.1 peritoneal exudate cells injected iv into CD45.2 mice infiltrated the iris after the intracameral injection of antigen. Mice receiving bindarit produced less CCL2 chemokine in aqueous humor after the intracameral injection of antigen and there was a decreased recruitment of monocytes into the AC.
Conclusions: :
The intracameral injection of antigen results in the infiltration of an inflammatory subset of monocytes into the anterior chamber where it is likely that they encounter antigen, recirculate and induce ACAID.
Keywords: ACAID • anterior chamber • immune tolerance/privilege