<b>Conclusion:</b> IL-17 plays a role in the pathogenesis of ocular surface and corneal disease and targeting this cytokine may provide a useful treatment option in the future.
To date, 5 of the identified loci, at ANAPC1, ADAMTS8, ADAMTS17, ABCA6, and COL6A1, have not previously been reported as associated with corneal disease.
Most notably, an intergenic variant close to ANAPC1 (rs78658973[A], frequency = 28.3%) strongly associates with decreased cell density and accounts for 24% of the population variance in cell density (β = -0.77 SD, P = 1.8 × 10<sup>-314</sup>) and associates with increased CH (β = 0.19 SD, P = 2.6 × 10<sup>-19</sup>) without affecting risk of corneal diseases and glaucoma.
However, due to the limited evidence, further research should be performed on the safety of anti-VEGF administration in patients with different corneal disorders.
Together, the results of these studies identify an essential role for IL-17-producing neutrophils and Th17 cells in regulating the growth of fungal hyphae and the severity of corneal disease.
Corneal disease is characterized by loss of corneal immunologic privilege and extensive neovascularization driven by vascular endothelial growth factor-A (VEGF-A).
Autosomal recessive congenital hereditary endothelial dystrophy (AR-CHED or CHED2) is a bilateral corneal disorder manifesting at birth or in early childhood.
Together with other results, our observation makes it unlikely that TGFBIp is imported into the cornea from the circulation as reported for other abundant extracellular corneal proteins and suggests corneal origin of TGFBIp deposits in individuals with inherited corneal diseases caused by mutations in the TGFBI gene.
Evidence against a blood derived origin for transforming growth factor beta induced protein in corneal disorders caused by mutations in the TGFBI gene.
To date, 5 of the identified loci, at ANAPC1, ADAMTS8, ADAMTS17, ABCA6, and COL6A1, have not previously been reported as associated with corneal disease.
Taken together, these data suggest that CD28 costimulation is required for HSK but that while initial infection of TG is greater in CD28<sup>-/-</sup> mice, this begins to normalize with time and this normalization is concurrent with the delayed development of antigen-specific CD8<sup>+</sup> T cells.<b>IMPORTANCE</b> We study the pathogenesis of herpes simplex virus-mediated corneal disease.
The over-expression of NLRP12 in B6 corneas significantly ameliorated the severity of corneal disease, bacterial burden, PMN infiltration and pro-inflammatory cytokine expression.
The downregulation of matrix metalloproteinase-2 and upregulation of alpha1-proteinase inhibitor by 17β-estradiol possibly serve as protective factor for the normal tomography in antagonizing the extracellular matrix degeneration in many cornea diseases.
In conclusion, the actin cytoskeleton regulatory pathway, MAPK and dilated cardiomyopathy signaling pathways, as well as CFL1 and ITGB6 genes, may be regulated by Srf to serve important roles in the progression of corneal disease.
Our data demonstrates that AAV5-Smad7 gene therapy is relatively safe with significant potential for the treatment of corneal disease currently resulting in fibrosis and impaired vision.
The realization of the importance of TRP channels acting as polymodal sensors of environmental stresses has identified potential drug targets for corneal disease.