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J. Alsalem, R. Susarla, M. M. Ahasan, M. Coca-Prados, R. Bland, E. A. Walker, S. Rauz, G. R. Wallace; A Role for 1,25(OH)2 Vitamin D3 in Ocular Immune Privilege?. Invest. Ophthalmol. Vis. Sci. 2010;51(13):4837.
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© ARVO (1962-2015); The Authors (2016-present)
Immune privilege is beneficial to the human eye as it serves to limit inflammatory reactions that could eventually cause blindness. Active vitamin D3, 1,25(OH)2D3 has been shown to play an important immunomodulatory role through the induction of antimicrobial peptides and anti-inflammatory responses in many cells. Studies in macrophages indicate that this may be mediated through stimulation of toll-like receptor-2/1 (TLR-2/1). Here we study the possible role of 1,25(OH)2D3 in ocular immune privilege.
Human adult retinal pigmented epithelial (ARPE-19), human corneal epithelial (HCE) and non-pigmented ciliary body epithelial (ODM2) cell lines were cultured. Gene expression and protein expression for elements of the vitamin D and Toll like receptor pathways were examined by conventional and real-time polymerase chain reaction (RT-PCR) and Western blot analysis both in the absence and presence of TLR2/1 ligand (Pam3cys). Immunohistochemical staining was also performed on paraffin-embedded sections of the anterior segments of normal human eye.
ARPE-19, HCE, and ODM2 cells expressed vitamin D receptor (VDR), and 25-Hydroxyvitamin D3 1-alpha-hydroxylase (CYP27B1) that converts 25-hydroxyvitamin D (25[OH]D) into 1,25(OH)2D3. Expression of the catabolizing enzyme, 24-hydoxylase (CYP24A1), was only detected in ARPE-19 and ODM2 cells. This was confirmed by the immunohistochemicaI staining of non-pigmented ciliary body epithelium. In addition, ARPE-19 cells expressed 1-alpha-hydroxylase and 24-hydoxylase proteins as shown by Western blot. Real time PCR analysis of ARPE-19 stimulated with Pam3cys demonstrated an upregulation of CYP27B1 (1.5 fold), VDR (2.5 fold), and CYP24A1 (5 fold) after 1, 2, and 6 hours respectively.
Our data show that ocular cells have the ability to convert inactive 25(OH)D into active 1,25(OH)2D3 and this can be upregulated by TLR stimulation. This suggests a possible role of vitamin D3 in ocular immune privilege.
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