author_facet Xu, H.
Xu, H.
author Xu, H.
spellingShingle Xu, H.
Acta Ophthalmologica
Retinal innate immune activation in health and disease
Ophthalmology
General Medicine
author_sort xu, h.
spelling Xu, H. 1755-375X 1755-3768 Wiley Ophthalmology General Medicine http://dx.doi.org/10.1111/j.1755-3768.2015.0155 <jats:title>Summary</jats:title><jats:p>Retina is considered as an immune privileged tissue, yet many inflammatory retinal diseases occur. Circulating immune cells are not able to freely migrate into the healthy retina due to the blood retina barrier. Retina is protected by its own innate immune system, including microglia, perivascular macrophages, a small number of dendritic cells and the complement system. When retina suffers from exogenous/endogenous insults, a well‐controlled innate immune response is initiated to maintain homeostasis and restore functionality, such response is therefore beneficial. Dysregulation or malfunction of the innate immune response may result in excessive production of inflammatory mediators that may contribute to retinal pathology. The presentation will discuss how innate immune response is controlled in the retina, and the potential contribution of uncontrolled or dysregulated innate immune activation to retinal lesion development in common sight‐threatening diseases such as age‐related retinal degeneration.</jats:p> Retinal innate immune activation in health and disease Acta Ophthalmologica
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title Retinal innate immune activation in health and disease
title_unstemmed Retinal innate immune activation in health and disease
title_full Retinal innate immune activation in health and disease
title_fullStr Retinal innate immune activation in health and disease
title_full_unstemmed Retinal innate immune activation in health and disease
title_short Retinal innate immune activation in health and disease
title_sort retinal innate immune activation in health and disease
topic Ophthalmology
General Medicine
url http://dx.doi.org/10.1111/j.1755-3768.2015.0155
publishDate 2015
physical
description <jats:title>Summary</jats:title><jats:p>Retina is considered as an immune privileged tissue, yet many inflammatory retinal diseases occur. Circulating immune cells are not able to freely migrate into the healthy retina due to the blood retina barrier. Retina is protected by its own innate immune system, including microglia, perivascular macrophages, a small number of dendritic cells and the complement system. When retina suffers from exogenous/endogenous insults, a well‐controlled innate immune response is initiated to maintain homeostasis and restore functionality, such response is therefore beneficial. Dysregulation or malfunction of the innate immune response may result in excessive production of inflammatory mediators that may contribute to retinal pathology. The presentation will discuss how innate immune response is controlled in the retina, and the potential contribution of uncontrolled or dysregulated innate immune activation to retinal lesion development in common sight‐threatening diseases such as age‐related retinal degeneration.</jats:p>
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author Xu, H.
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description <jats:title>Summary</jats:title><jats:p>Retina is considered as an immune privileged tissue, yet many inflammatory retinal diseases occur. Circulating immune cells are not able to freely migrate into the healthy retina due to the blood retina barrier. Retina is protected by its own innate immune system, including microglia, perivascular macrophages, a small number of dendritic cells and the complement system. When retina suffers from exogenous/endogenous insults, a well‐controlled innate immune response is initiated to maintain homeostasis and restore functionality, such response is therefore beneficial. Dysregulation or malfunction of the innate immune response may result in excessive production of inflammatory mediators that may contribute to retinal pathology. The presentation will discuss how innate immune response is controlled in the retina, and the potential contribution of uncontrolled or dysregulated innate immune activation to retinal lesion development in common sight‐threatening diseases such as age‐related retinal degeneration.</jats:p>
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spelling Xu, H. 1755-375X 1755-3768 Wiley Ophthalmology General Medicine http://dx.doi.org/10.1111/j.1755-3768.2015.0155 <jats:title>Summary</jats:title><jats:p>Retina is considered as an immune privileged tissue, yet many inflammatory retinal diseases occur. Circulating immune cells are not able to freely migrate into the healthy retina due to the blood retina barrier. Retina is protected by its own innate immune system, including microglia, perivascular macrophages, a small number of dendritic cells and the complement system. When retina suffers from exogenous/endogenous insults, a well‐controlled innate immune response is initiated to maintain homeostasis and restore functionality, such response is therefore beneficial. Dysregulation or malfunction of the innate immune response may result in excessive production of inflammatory mediators that may contribute to retinal pathology. The presentation will discuss how innate immune response is controlled in the retina, and the potential contribution of uncontrolled or dysregulated innate immune activation to retinal lesion development in common sight‐threatening diseases such as age‐related retinal degeneration.</jats:p> Retinal innate immune activation in health and disease Acta Ophthalmologica
spellingShingle Xu, H., Acta Ophthalmologica, Retinal innate immune activation in health and disease, Ophthalmology, General Medicine
title Retinal innate immune activation in health and disease
title_full Retinal innate immune activation in health and disease
title_fullStr Retinal innate immune activation in health and disease
title_full_unstemmed Retinal innate immune activation in health and disease
title_short Retinal innate immune activation in health and disease
title_sort retinal innate immune activation in health and disease
title_unstemmed Retinal innate immune activation in health and disease
topic Ophthalmology, General Medicine
url http://dx.doi.org/10.1111/j.1755-3768.2015.0155