PURPOSE. Idiopathic inflammation of the cornea, keratitis, has been propose
d to result from an autoimmune process, but thus far no convenient animal m
odel of keratitis exists. An attempt was made to establish an animal model
for keratitis, to investigate possible autoimmune mechanisms.
METHODS. T-cell lines were established from lymph node cells removed from r
ats immunized with bovine corneal epithelium (BCE) extract. After restimula
tion in vitro with BCE or a specific corneal antigen, the cells were transf
erred by intraperitoneal injection into naive rats, rats subjected to total
body irradiation, or rats in which only one eye was irradiated.
RESULTS. Neither direct immunization with corneal antigens nor transfer of
activated anti-corneal T-cells into naive rats gave any signs of keratitis.
Irradiation alone did not induce corneal inflammation. Transfer of corneal
-specific activated T cells into irradiated rats produced keratitis startin
g around day 4 and culminating around day 8. The disease was self-limiting
and the severity dependent on the dose and site of radiation. Keratitis was
characterized by corneal haze, conjunctival and episcleral hyperemia, epis
cleral hemorrhages, chemosis, corneal infiltrates, and vascularization. Imm
unohistochemistry showed T-cell and macrophage infiltration of epithelium a
nd stroma in the affected corneas.
CONCLUSIONS. Thus, keratitis may be produced by T cells reactive to corneal
antigens, provided that the target tissue has been made susceptible by irr
adiation. The effectiveness of T-cell vaccination in preventing adoptive ke
ratitis suggests that systemic as well as local tissue factors may regulate
the disease process.