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,
Departments of
* Dermatology and
Ophthalmology, Harvard Medical School, Boston, MA 02114; and
Department of Medicine, Pulmonary Division, Brigham and Women’s Hospital, Boston, MA 02115
Anterior chamber-associated immune deviation (ACAID), a
manifestation of ocular immune privilege, prevents Th1-dependent
delayed hypersensitivity from developing in response to eye-derived
Ags, thereby preserving vision. Since Th2-type cells have recently been
shown to mediate destructive inflammation of the cornea, we wondered
whether pre-emptive induction of ACAID could inhibit Th2 responses.
Using a murine model of OVA -specific, Th2-dependent pulmonary
inflammation, we pretreated susceptible mice by injecting OVA alone
into the anterior chamber, or by injecting OVA-pulsed, TGF-
2-treated
peritoneal exudate cells i.v. These mice were then immunized with OVA
plus alum strategy that generates Th2-mediated OVA-specific pulmonary
pathology. When pretreated mice were challenged intratracheally with
OVA, their bronchoalveolar lavage fluids contained far fewer
eosinophils and significantly less IL-4, IL-5, and IL-13 compared with
that of positive, nonpretreated controls. Similarly, lung-draining
lymph node cells of pretreated mice secreted significantly less IL-4,
IL-5, and IL-13 when challenged in vitro with OVA. Moreover, sera from
pretreated mice contained much lower titers of OVA-specific IgE Abs. We
conclude that Ags injected into the anterior chamber of the eye impair
both Th1 and Th2 responses. These results reduce the likelihood that
ACAID regulates Th1 responses via a Th2-like mechanism. Thus, immune
privilege of the eye regulates inflammation secondary to both Th1- and
Th2-type immune responses.
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