Journal article
Immune Responses in the Glaucomatous Retina: Regulation and Dynamics
Cells (Basel, Switzerland), Vol.10(1973), p.1973
08/01/2021
DOI: 10.3390/cells10081973
PMCID: PMC8391899
PMID: 34440742
Abstract
Glaucoma is a multifactorial disease resulting in progressive vision loss due to retinal ganglion cell (RGC) dysfunction and death. Early events in the pathobiology of the disease include oxidative, metabolic, or mechanical stress that acts upon RGC, causing these to rapidly release danger signals, including extracellular ATP, resulting in micro- and macroglial activation and neuroinflammation. Danger signaling also leads to the formation of inflammasomes in the retina that enable maturation of proinflammatory cytokines such IL-1β and IL-18. Chronic neuroinflammation can have directly damaging effects on RGC, but it also creates a proinflammatory environment and compromises the immune privilege of the retina. In particular, continuous synthesis of proinflammatory mediators such as TNFα, IL-1β, and anaphylatoxins weakens the blood–retina barrier and recruits or activates T-cells. Recent data have demonstrated that adaptive immune responses strongly exacerbate RGC loss in animal models of the disease as T-cells appear to target heat shock proteins displayed on the surface of stressed RGC to cause their apoptotic death. It is possible that dysregulation of these immune responses contributes to the continued loss of RGC in some patients.
Details
- Title: Subtitle
- Immune Responses in the Glaucomatous Retina: Regulation and Dynamics
- Creators
- Valery I. Shestopalov - Department of Ophthalmology, Miller School of Medicine, University of Miami, Miami, FL 33101, USAMarkus Spurlock - Department of Cell and Developmental Biology, Miller School of Medicine, University of Miami, Miami, FL 33101, USAOliver W. Gramlich - Department of Veterans Affairs, Center for the Prevention and Treatment of Visual Loss, Iowa City, IA 52246, USAMarkus H. Kuehn - Department of Veterans Affairs, Center for the Prevention and Treatment of Visual Loss, Iowa City, IA 52246, USA
- Resource Type
- Journal article
- Publication Details
- Cells (Basel, Switzerland), Vol.10(1973), p.1973
- DOI
- 10.3390/cells10081973
- PMID
- 34440742
- PMCID
- PMC8391899
- NLM abbreviation
- Cells
- eISSN
- 2073-4409
- Publisher
- MDPI AG
- Grant note
- DOI: 10.13039/100006380, name: Rehabilitation Research and Development Service, award: I50 RX003002, I01 RX002860-01; DOI: 10.13039/100000002, name: National Institutes of Health, award: EY032261; DOI: 10.13039/100000005, name: U.S. Department of Defense, award: VR200079
- Language
- English
- Date published
- 08/01/2021
- Academic Unit
- Iowa Neuroscience Institute; Neuroscience and Pharmacology; Ophthalmology and Visual Sciences
- Record Identifier
- 9984125622102771
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