ArticleJournal of neuroinflammation2023
Assessing the role of T cells in response to retinal injury to uncover new therapeutic targets for the treatment of retinal degeneration.
Article in Journal of neuroinflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 19 citations in OpenAlex.
- Cell-intrinsic vulnerability and immune activation cooperate to drive degeneration in a mitochondrial complex I deficiency model of optic neuropathy.Journal of neuroinflammation · 2026Article
- Regulation of Adult Zebrafish Retinal Regeneration by Lamβ1b-Chain-Containing Laminins.bioRxiv : the preprint server for biology · 2025Article
- Alzheimer's disease and age-related macular degeneration: Shared and distinct immune mechanisms.Immunity · 2025Review
- Article
- Plasma Interferon-gamma is Associated with Poor Treatment Response in Neovascular Age-Related Macular Degeneration.Aging and disease · 2025Article
- Unraveling the immune response in optic nerve injury: implications for retinal ganglion cell protection.Frontiers in immunology · 2025Review
- Outer retina micro-inflammation is driven by T cell responses prior to retinal degeneration in early age-related macular degeneration.Frontiers in immunology · 2025Article
- Macrophages coordinate immune response to laser-induced injury via extracellular traps.Journal of neuroinflammation · 2024Article
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Authors and funding
6 authors at 5 institutions in 2 countries.
Funding
Abstract
backgroundRetinal degeneration is a disease affecting the eye, which is an immune-privileged site because of its anatomical and physiological properties. Alterations in retinal homeostasis-because of injury, disease, or aging-initiate inflammatory cascades, where peripheral leukocytes (PL) infiltrate the parenchyma, leading to retinal degeneration. So far, research on PL's role in retinal degeneration was limited to observing a few cell types at specific times or sectioning the tissue. This restricted our understanding of immune cell interactions and response duration.
methodsIn vivo microscopy in preclinical mouse models can overcome these limitations enabling the spatio-temporal characterization of PL dynamics. Through in vivo imaging, we assessed structural and fluorescence changes in response to a focal injury at a defined location over time. We also utilized minimally invasive techniques, pharmacological interventions, and knockout (KO) mice to determine the role of PL in local inflammation. Furthermore, we investigated PL abundance and localization during retinal degeneration in human eyes by histological analysis to assess to which extent our preclinical study translates to human retinal degeneration.
resultsWe demonstrate that PL, especially T cells, play a detrimental role during retinal injury response. In mice, we observed the recruitment of helper and cytotoxic T cells in the parenchyma post-injury, and T cells also resided in the macula and peripheral retina in pathological conditions in humans. Additionally, we found that the pharmacological PL reduction and genetic depletion of T-cells reduced injured areas in murine retinas and rescued the blood-retina barrier (BRB) integrity. Both conditions promoted morphological changes of Cx3cr1
conclusionsOur data provide novel insights into the adaptive immune response to retinal injury in mice and human retinal degeneration. Such information is fundamental to understanding retinal disorders and developing therapeutics to modulate immune responses to retinal degeneration safely.
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