Journal
NATURE COMMUNICATIONS
Volume 9, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41467-018-05681-9
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Funding
- National Institutes of Health [EY025913, EY027067, EY025259, NS038253, AI69208]
- Lion's Foundation
- Miriam and Sheldon Adelson Medical Research Foundation
- National Nature Science Foundation of China [81200683, 20120162]
- Ivan R. Cottrell Professorship and Research Fund
- Oogfonds/StichtingGlaucoomfonds/SNOO/LOOF/Nelly Reef Fund/Prins Bernhard Cultuur Fonds
- Koch Institute Support (core) Grant from the National Cancer Institute [P30-CA14051]
- NEI [P30 EY03790]
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Glaucoma is the most prevalent neurodegenerative disease and a leading cause of blindness worldwide. The mechanisms causing glaucomatous neurodegeneration are not fully understood. Here we show, using mice deficient in T and/or B cells and adoptive cell transfer, that transient elevation of intraocular pressure (IOP) is sufficient to induce T-cell infiltration into the retina. This T-cell infiltration leads to a prolonged phase of retinal ganglion cell degeneration that persists after IOP returns to a normal level. Heat shock proteins (HSP) are identified as target antigens of T-cell responses in glaucomatous mice and human glaucoma patients. Furthermore, retina-infiltrating T cells cross-react with human and bacterial HSPs; mice raised in the absence of commensal microflora do not develop glaucomatous T-cell responses or the associated neurodegeneration. These results provide compelling evidence that glaucomatous neurodegeneration is mediated in part by T cells that are pre-sensitized by exposure to commensal microflora.
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