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Scheme of the ray path reaching the extremity of the retina at the ora serrata, at an angle of 50.77°.
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One and half decades ago, Müller glia cells of the retina became subjects of extended research as optical waveguides. It was demonstrated that outside the fovea, these cells are capable of providing light transmission through the thicker parts of the retina from the vitreous surface to the photoreceptor cells. We combined optical modeling of the ey...
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Background
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Citations
... Additionally, microglia release cytokines that attract T-cells to the retinal parenchyma, thereby contributing to immune responses in retinal degenerative diseases (Ramirez et al., 2017). Müller cells span the entire depth of the retina, contributing to light transmission and maintaining homeostasis under physiological conditions (Szabó et al., 2022;Yoshimoto et al., 2023). In response to retinal degeneration, they exhibit reactivity to protect the retina from further damage and promote repair following pathological insult. ...
Glia antigen-presenting cells (APCs) are pivotal regulators of immune surveillance within the retina, maintaining tissue homeostasis and promptly responding to insults. The intricate mechanisms underlying their local coordination and activation remain unclear.
Our study integrates an animal model of retinal injury, retrospective analysis of human retinas, and in vitro experiments to elucidate insights into the pivotal role of antigen presentation in neuroimmunology during retinal degeneration, uncovering the involvement of various glial cells, notably Müller glia, and microglia. Glial cells act as sentinels, detecting antigens released during degeneration and interacting with T-cells via MHC molecules, which are essential for immune responses. Microglia function as APCs via the MHC class II pathway, upregulating key molecules such as Csf1r and cytokines. In contrast, Müller cells act as atypical APCs through the MHC class I pathway, exhibiting upregulated antigen processing genes and promoting a CD8 ⁺ T-cell response. Distinct cytokine signaling pathways, including TNF-α and IFN, contribute to the immune balance. Human retinal specimens corroborate these findings, demonstrating glial activation and MHC expression correlating with degenerative changes. In vitro assays also confirmed differential T-cell migration responses to activated microglia and Müller cells, highlighting their role in shaping the immune milieu within the retina. These insights emphasize the complex interplay between glial cells and T-cells, influencing the inflammatory environment and potentially modulating degenerative processes.
In summary, our study emphasizes the involvement of retinal glial cells in modulating the immune response after insults to the retinal parenchyma. Thus, unraveling the intricacies of glia-mediated antigen presentation in retinal degeneration is essential for developing precise therapeutic interventions for retinal pathologies.
Glia antigen‐presenting cells (APCs) are pivotal regulators of immune surveillance within the retina, maintaining tissue homeostasis and promptly responding to insults. However, the intricate mechanisms underlying their local coordination and activation remain unclear. Our study integrates an animal model of retinal injury, retrospective analysis of human retinas, and in vitro experiments to gain insights into the crucial role of antigen presentation in neuroimmunology during retinal degeneration (RD), uncovering the involvement of various glial cells, notably Müller glia and microglia. Glial cells act as sentinels, detecting antigens released during degeneration and interacting with T‐cells via MHC molecules, which are essential for immune responses. Microglia function as APCs via the MHC Class II pathway, upregulating key molecules such as Csf1r and cytokines. In contrast, Müller cells act through the MHC Class I pathway, exhibiting upregulated antigen processing genes and promoting a CD8 ⁺ T‐cell response. Distinct cytokine signaling pathways, including TNF‐α and IFN Type I, contribute to the immune balance. Human retinal specimens corroborate these findings, demonstrating glial activation and MHC expression correlating with degenerative changes. In vitro assays also confirmed differential T‐cell migration responses to activated microglia and Müller cells, highlighting their role in shaping the immune milieu within the retina. In summary, our study emphasizes the involvement of retinal glial cells in modulating the immune response after insults to the retinal parenchyma. Unraveling the intricacies of glia‐mediated antigen presentation in RD is essential for developing precise therapeutic interventions for retinal pathologies.
