I cannot obviously speak for the specific case you mention (and, anyway, I am not a medical doctor so I would not make a diagnosis in any case), but one thing that comes to mind is that eyes are part of the immunologically privileged sites of the body. This means that an inflammatory response is not elicited in case of the introduction of an antigen.
I quote from Immunobiology by Charles Janeway
Some body sites are immunologically privileged. Tissue grafts placed in these sites often last indefinitely, and antigens placed in these sites do not elicit destructive immune responses.
Paradoxically, the antigens sequestered in immunologically privileged sites are often the targets of autoimmune attack; for example, brain autoantigens such as myelin basic protein are targeted in multiple sclerosis. It is therefore clear that this antigen does not induce tolerance due to clonal deletion of the self-reactive T cells. Mice only become diseased when they are deliberately immunized with myelin basic protein, in which case they become acutely sick, show severe infiltration of the brain with specific TH1 cells, and often die.
Thus, at least some antigens expressed in immunologically privileged sites induce neither tolerance nor activation, but if activation is induced elsewhere they can become targets for autoimmune attack (see Section 13-25). It seems plausible that T cells specific for antigens sequestered in immunologically privileged sites are more likely to remain in a state of immunological ignorance. Further evidence for this comes from the eye disease sympathetic ophthalmia (Fig. 13.36). If one eye is ruptured by a blow or other trauma, an autoimmune response to eye proteins can occur, although this happens only rarely. Once the response is induced, it often attacks both eyes. Immuno-suppression and removal of the damaged eye, the source of antigen, is frequently required to preserve vision in the undamaged eye.
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