Purchase this article with an account.
C. S. Hwang, S. Yeh, C. S. De Paiva, K. Trinca, A. Lingappan, J. K. Rafati, W. J. Farley, D.-Q. Li, S. C. Pflugfelder; Spontaneous Meibomianitis in AIRE-Deficient Mice. Invest. Ophthalmol. Vis. Sci. 2009;50(13):5517.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
Patients with autoimmune polyendocrinopathy (APECED), a condition that results from a mutation in the Autoimmune Regulatory (Aire) gene, develop chronic ocular surface inflammatory disease, including meibomianitis. The purpose of this study is to examine the meibomian gland immunopathology in Aire-knockout and wild type mice.
Eyes with corresponding lids from Aire-deficient and wild type (C57BL6/J) mice were surgically removed, frozen, sectioned, and stained for immune/inflammatory cell markers (CD4+, CD8+, CD11b+, CD45+) by immunohistochemistry. The densities of these cells were measured in the meibomian glands of these tissues.
There was a greater density of CD4+, CD11b+, and CD45+ in the meibomian glands of Aire-deficient mice compared to the wild-type mice (p < 0.01, p < 0.01, p < 0.001 respectively). In contrast, the number of CD8+ cells was significantly higher in the meibomian glands of wild type mice compared to Aire-deficient mice (p < 0.001).
The meibomian glands in Aire-deficient mice have a more immunologically active environment compared to wild type mice. Defective immunoregulation in the Aire glands may be related to the lower density of CD8+ cells. The altered immune environment may be the basis for the chronic meibomianitis and ocular surface disease observed in APECED patients.
This PDF is available to Subscribers Only