2022

DOI: 10.1016/j.heliyon.2022.e08973

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A histological study of atherosclerotic characteristics in age-related macular degeneration

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Discussion2

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General Pathogenesis Of Dry Amd1

The Role Of Ripk In Retinal Degeneration and Neuroinflammation1

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Cited by 8 publications

(9 citation statements)

References 59 publications

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“…We constructed LASSO regression models using the R package “glmnet” to analyze the diagnostic contributions of these 18 IGPs. LASSO played a crucial role in implementing measures to prevent overfitting, ensuring the robustness and generalizability of the model [ 36 ]. As depicted in Fig.…”

Section: Resultsmentioning

confidence: 99%

Serum N-glycomic profiling identifies candidate biomarker panels for assessing coronary artery stenosis severity

Wu,

Liu,

Xu

et al. 2024

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No abstract

“…We constructed LASSO regression models using the R package “glmnet” to analyze the diagnostic contributions of these 18 IGPs. LASSO played a crucial role in implementing measures to prevent overfitting, ensuring the robustness and generalizability of the model [ 36 ]. As depicted in Fig.…”

Section: Resultsmentioning

confidence: 99%

Serum N-glycomic profiling identifies candidate biomarker panels for assessing coronary artery stenosis severity

Wu,

Liu,

Xu

et al. 2024

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No abstract

“…A limiting factor is the relative insufficient knowledge of the specific role of the different immune cell types within the retinal inflammatory orchestra that leads to tissue degeneration. Genetic investigations [ 62 ], alongside human histological data and animal studies [ 63 , 64 ], have predominantly concentrated on the involvement of innate immunity in mediating cellular death during the progression of retinal degeneration. Upon injury, macrophages/monocytes are activated, and their reactivity can be harmful as well as beneficial, depending on the surrounding milieu.…”

Section: Discussionmentioning

confidence: 99%

Macrophages coordinate immune response to laser-induced injury via extracellular traps

Conedera,

Kokona,

Zinkernagel

et al. 2024

J Neuroinflammation

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Background Retinal degeneration results from disruptions in retinal homeostasis due to injury, disease, or aging and triggers peripheral leukocyte infiltration. Effective immune responses rely on coordinated actions of resident microglia and recruited macrophages, critical for tissue remodeling and repair. However, these phagocytes also contribute to chronic inflammation in degenerated retinas, yet the precise coordination of immune response to retinal damage remains elusive. Recent investigations have demonstrated that phagocytic cells can produce extracellular traps (ETs), which are a source of self-antigens that alter the immune response, which can potentially lead to tissue injury. Methods Innovations in experimental systems facilitate real-time exploration of immune cell interactions and dynamic responses. We integrated in vivo imaging with ultrastructural analysis, transcriptomics, pharmacological treatments, and knockout mice to elucidate the role of phagocytes and their modulation of the local inflammatory response through extracellular traps (ETs). Deciphering these mechanisms is essential for developing novel and enhanced immunotherapeutic approaches that can redirect a specific maladaptive immune response towards favorable wound healing in the retina. Results Our findings underscore the pivotal role of innate immune cells, especially macrophages/monocytes, in regulating retinal repair and inflammation. The absence of neutrophil and macrophage infiltration aids parenchymal integrity restoration, while their depletion, particularly macrophages/monocytes, impedes vascular recovery. We demonstrate that macrophages/monocytes, when recruited in the retina, release chromatin and granular proteins, forming ETs. Furthermore, the pharmacological inhibition of ETosis support retinal and vascular repair, surpassing the effects of blocking innate immune cell recruitment. Simultaneously, the absence of ETosis reshapes the inflammatory response, causing neutrophils, helper, and cytotoxic T-cells to be restricted primarily in the superficial capillary plexus instead of reaching the damaged photoreceptor layer. Conclusions Our data offer novel insights into innate immunity's role in responding to retinal damage and potentially help developing innovative immunotherapeutic approaches that can shift the immune response from maladaptive to beneficial for retinal regeneration.

“…A limiting factor is the relative insufficient knowledge of the specific role of the different immune cell types within the retinal inflammatory orchestra that leads to tissue degeneration. Genetic investigations (56), alongside human histological data and animal studies (57, 58), have pre-dominantly concentrated on the involvement of innate immunity in mediating cellular death during the progression of retinal degeneration. Upon injury, macrophages/monocytes are activated, and their reactivity can be harmful as well as beneficial, depending on the surrounding milieu.…”

Section: Discussionmentioning

confidence: 99%

Macrophages Coordinate Immune Response to Laser-Induced Injury via Extracellular Traps

Conedera,

Kokona,

Zinkernagel

et al. 2023

Preprint

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Macrophages/monocytes, the primary contributors to chronic inflammation in degenerated retinas, orchestrate intricate immune responses. They remain enigmatic in their local coordination and activation mechanisms. Innovations in experimental systems enable real-time exploration of immune cell interactions and temporal dimensions in response. In preclinical mouse models, we use in vivo microscopy to unravel how macrophages/monocytes govern microglia and PL responses spatio-temporally. Our findings underscore the pivotal role of innate immune cells, especially macrophages/monocytes, in regulating retinal repair. The absence of neutrophil and macrophage infiltration aids parenchymal integrity restoration, while their depletion, particularly macrophages/monocytes, impedes vascular recovery. Innate immune cells, when activated, release chromatin and granular proteins, forming extracellular traps (ETs), critical for tissue repair by modulating neutrophil and T-cell responses. Our investigations demonstrate that pharmacological inhibition of ETosis with Cl-amidine enhances retinal and vascular repair, surpassing the effects of blocking innate immune cell recruitment. Simultaneously, Cl-amidine treatment reshapes the inflammatory response, causing neutrophils, helper, and cytotoxic T-cells to cluster primarily in the superficial capillary plexus, affecting retinal microvasculature perfusion. Our data offer novel insights into innate immunity's role in responding to retinal damage, potentially informing more effective immunotherapeutic strategies for neurodegenerative diseases.

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