期刊
MUCOSAL IMMUNOLOGY
卷 7, 期 2, 页码 417-427出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/mi.2013.61
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资金
- NIH [EY018888, EY11915, EY018090, EY002520, EY020799]
- Research to Prevent Blindness
- Oshman Foundation
- William Stamps Farish Fund
- Hamill Foundation
- Cytometry and Cell Sorting Core at Baylor College of Medicine
- NIH NIAID [P30AI036211]
- NCI [P30CA125123]
- NCRR [S10RR024574]
This study investigated the regulatory function of CD8(+) cells in T helper-17 (Th17) cell-mediated corneal epithelial barrier disruption that develops in a murine desiccating stress (DS) model that resembles Sjogren syndrome. CD8(+) cell depletion promoted generation of interleukin-17A (IL-17A)-producing CD4(+) T cells via activation of dendritic cells in both the ocular surface and draining cervical lymph nodes in C57BL/6 mice subjected to DS. T-cell-deficient nude recipient mice receiving adoptively transferred CD4(+) T cells from CD8(+) cell-depleted donors exposed to DS displayed increased CD4(+) T-cell infiltration and elevated IL-17A and CC-chemokine attractant ligand 20 levels in the ocular surface, which was associated with greater corneal barrier disruption. Enhanced DS-specific corneal barrier disruption in CD8-depleted donor mice correlated with a Th17-mediated expression of matrix metalloproteinases (MMP-3 and MMP-9) in the recipient corneal epithelium. Co-transfer of CD8(+)CD103(+) regulatory T cells did not affect the ability of DS-specific pathogenic CD4(+) T cells to infiltrate and cause ocular surface disease in the nude recipients, showing that CD8(+) cells regulate the efferent arm of DS-induced immune response. In summary, CD8(+) regulatory cells suppress generation of a pathogenic Th17 response that has a pivotal role in DS-induced disruption of corneal barrier function.
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