Characterization of intraocular immunopathology following intracameral inoculation with alloantigen

Anterior chamber-associated immune deviation (ACAID) is a form of peripheral tolerance achieved via intracameral antigen inoculation. It is well known that ACAID effectively down-regulates potentially destructive immunities such as delayed-type hypersensitivity (DTH) at extraorbital sites. However, what has not been specifically addressed is whether local intraocular tissues are negatively affected from intracamerally placed antigen. Thus, the current study was undertaken to detect and characterize potential pathological effects on intraocular tissues following intracameral inoculation with alloantigen.

ACAID induced in C57BL/6 hosts via intracameral inoculation with allogeneic (BALB/c) splenocytes was confirmed by the absence of DTH reactivity in the periphery. Injuries to the anterior segment and neuroretina following intracameral inoculation were evaluated pathologically via histological evaluation, molecularly via upregulation of glial fibrillary acidic protein (GFAP), and functionally via assessment of photoreceptor degeneration and electroretinogram (ERG) out to 24 days. In all experiments, intracamerally inoculated mice were compared to sham-operated, and controlled lens-punctured mice--a procedure that elicits intracameral inflammation for positive identification of immunopathological changes.

Inflammation of anterior segment tissues persisted out to eight days, despite evidence that significant clearance of allogeneic cells took place within 6 h. In the neuroretina, a transient loss in ERG B-wave amplitudes was detected, but photoreceptor degeneration and GFAP upregulation were not.

Intracameral inoculation with alloantigen leads to anterior segment inflammation and ERG dysfunction; however, this was markedly reduced and transient when compared to strong anterior segment inflammation induced by a more serious lens-puncture wound.