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1 From the Laboratory of Immunology and the 2 Laboratory of Retinal Cell and Molecular Biology, National Eye Institute, National Institutes of Health, Bethesda, Maryland.
PURPOSE. Experimental autoimmune uveoretinitis (EAU) in mice is an important model for elucidating basic mechanisms in autoimmune eye disease. The need for pertussis toxin (PTX) as an additional adjuvant to elicit EAU has limited the usefulness of this model in some types of studies by introducing a pleiotropic factor with confounding effects on the immune response.
METHODS. In the present study the authors examined the ability of B10.RIII mice, the most susceptible strain known so far, to develop EAU in response to the retinal antigen, interphotoreceptor retinoid-binding protein (IRBP), and to a major uveitogenic epitope of IRBP, peptide (p)161-180, in the absence of PTX treatment.
RESULTS. The data indicate that high disease scores in response to IRBP and
p161-180 were found in B10.RIII mice, without the need for PTX as part
of the immunization protocol. Unlike the B10.A strain in which
appreciable disease did not develop without PTX, B10.RIII mice mounted
a high IFN-
response to IRBP in the absence of PTX treatment.
Interestingly, and unlike the effect with IRBP, in vitro recall
response to p161-180 was low in IFN-, despite good EAU scores.
CONCLUSIONS. The data indicate that an important mechanism through which PTX
facilitates induction of cell-mediated autoimmunity is by promoting a
Th1 polarization of the immune response. The propensity of B10.RIII
mice to mount a more polarized Th1 response to IRBP than other strains
may contribute to their ability to develop EAU without pertussis
adjuvant. Nevertheless, the induction of EAU by p161-180 in the context
of a relatively limited IFN- production indicates that non–Th1- and
Th-related mechanisms are likely to act in concert to determine the
outcome of disease.
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