Edited by:
Professor Thomas Langmann, PhD, University of Cologne, Germany
Professor Przemyslaw (Mike) Sapieha, PhD, University of Montreal, Canada
This collection is no longer accepting submissions.
Journal of Neuroinflammation is calling for submissions to our new Collection on "Neuroinflammation in the Retina".
Image credit: Prof. Langmann
‘Wet’ age-related macular degeneration (AMD) is characterized by pathologic choroidal neovascularization (CNV) that destroys central vision. Abundant evidence points to inflammation and immune cell dysfunction...
The IL-6 cytokine family, with its crucial and pleiotropic intracellular signaling pathway STAT3, is a promising target for treating vasoproliferative retinal diseases. Previous research has shown that IL-6 ci...
Ischemic retinopathies including diabetic retinopathy are major causes of vision loss. Inner blood-retinal barrier (BRB) breakdown with retinal vascular hyperpermeability results in macular edema. Although dys...
Retinitis pigmentosa (RP), an inherited retinal disease, affects 1,5 million people worldwide. The initial mutation-driven photoreceptor degeneration leads to chronic inflammation, characterized by Müller cell...
Ischemia-induced retinopathy is a hallmark finding of common visual disorders including diabetic retinopathy (DR) and central retinal artery and vein occlusions. Treatments for ischemic retinopathies fail to i...
The eye is a highly specialized sensory organ which encompasses the retina as a part of the central nervous system, but also non-neural compartments such as the transparent vitreous body ensuring stability of ...
The microglia-mediated neuroinflammation have been shown to play a crucial role in the ocular pathological angiogenesis process, but specific immunotherapies for neovascular ocular diseases are still lacking. ...
Radiation retinopathy (RR) is a major side effect of ocular tumor treatment by plaque brachytherapy or proton beam therapy. RR manifests as delayed and progressive microvasculopathy, ischemia and macular edema...
Recent experimental studies of neuroinflammation in glaucoma pointed to cFLIP as a molecular switch for cell fate decisions, mainly regulating cell type-specific caspase-8 functions in cell death and inflammat...
Autoimmune uveitis is a leading cause of severe vision loss, and animal models provide unique opportunities for studying its pathogenesis and therapeutic strategies. Here we employ scRNA-seq, RNA-seq and vario...
Behcet’s disease (BD) is a rare but globally distributed vasculitis that primarily affects populations in the Mediterranean and Asian regions. Behcet’s uveitis (BU) is a common manifestation of BD, occurring i...
The human gut microbiome (GM) is involved in inflammation and immune response regulation. Dysbiosis, an imbalance in this ecosystem, facilitates pathogenic invasion, disrupts immune equilibrium, and potentiall...
NADPH oxidase (NOX), a primary source of endothelial reactive oxygen species (ROS), is considered a key event in disrupting the integrity of the blood-retinal barrier. Abnormalities in neurovascular-coupled im...
Neovascular age-related macular degeneration (nAMD), accounts for up to 90% of AMD-associated vision loss, ultimately resulting in the formation of fibrotic scar in the macular region. The pathogenesis of subr...
The retinal pigment epithelium (RPE) maintains photoreceptor viability and function, completes the visual cycle, and forms the outer blood-retinal barrier (oBRB). Loss of RPE function gives rise to several mon...
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 r...
Myeloid cells including microglia and macrophages play crucial roles in retinal homeostasis by clearing cellular debris and regulating inflammation. These cells are activated in several blinding ischemic retin...
Age-related macular degeneration (AMD) is a leading cause of irreversible vision loss, characterised by the dysfunction and death of the photoreceptors and retinal pigment epithelium (RPE). Innate immune cell ...
Inherited, age-related, and acute retinal diseases are often exacerbated by an aberrant or excessive activity of the complement system. Consequently, cells not directly affected by an acute event or genetic va...
Glaucoma is a complex neurodegenerative disorder characterized by the progressive loss of retinal ganglion cells (RGC) and optic nerve axons, leading to irreversible visual impairment. Despite its clinical sig...
Diabetic retinopathy (DR) affects about 200 million people worldwide, causing leakage of blood components into retinal tissues, leading to activation of microglia, the resident phagocytes of the retina, promot...
Diabetic retinopathy (DR) is considered a primarily microvascular complication of diabetes. Müller glia cells are at the centre of the retinal neurovascular unit and play a critical role in DR. We therefore in...
Age-related macular degeneration (AMD) is invariably associated with the chronic accumulation of activated mononuclear phagocytes in the subretinal space. The mononuclear phagocytes are composed of microglial ...
Pathological neovascularization is a pivotal biological process in wet age-related macular degeneration (AMD), retinopathy of prematurity (ROP) and proliferative diabetic retinopathy (PDR), in which macrophage...
Neuroinflammation and mitochondrial dysfunction play crucial roles in retinal ischemia and reperfusion (IR) injury. Recent studies have identified mitochondrial function as a promising target for immunomodulat...
Vision loss in patients with wet/exudative age-related macular degeneration (AMD) is associated with choroidal neovascularization (CNV), and AMD is the leading cause of irreversible vision impairment in older ...
Neovascular age-related macular degeneration causes vision loss from destructive angiogenesis, termed choroidal neovascularization (CNV). Cx3cr1−/− mice display alterations in non-classical monocytes and microgli...
Retinal degenerative and neovascular diseases, including age-related macular degeneration (AMD), diabetic retinopathy (DR), glaucoma and rare monogenic dystrophies are major causes for global severe vision loss or blindness. In recent years, neuroinflammatory mechanisms have been identified as major factors for triggering the onset and progression of all these retinal diseases. Loss of retinal immune homeostasis is often accompanied by profound changes in cellular and humoral innate immunity and also involves adaptive immune responses by invading blood cell populations. We are only just beginning to understand the complex ocular inflammatory mechanisms and interplay between immune cells that occur in the eyes of patients with visual impairment.
This Collection seeks to discover novel immune mechanisms in the diseased retina that may offer novel diagnostic markers or highlight targets for immuno-modulatory therapies that could help to reduce the burden of vision loss worldwide.
As part of this Collection, we invite articles that cover the following topics:
• Role of resident and invading mononuclear phagocytes in the retina
• Role of T-cells and B-cells in retinal disease
• Complement factors in retinal disease
• Retinal pigment epithelium (RPE) inflammasome
• Immune responses in retinal gene therapy
• Microbiome and retinal immunity
• Retinal Immune memory and epigenetics
• Cellular senescence and retinal immune system
• Microglia-glia interactions in the retina
This Collection welcomes submission of original Research Articles and Reviews. Should you wish to submit a different article type, please read our submission guidelines to confirm that type is accepted by the journal. Articles for this Collection should be submitted via our submission system, Snapp. During the submission process you will be asked whether you are submitting to a Collection, please select "Neuroinflammation in the Retina" from the dropdown menu.
Articles will undergo the journal’s standard peer-review process and are subject to all of the journal’s standard policies. Articles will be added to the Collection as they are published.
The Guest Editors have no competing interests with the submissions which they handle through the peer review process. The peer review of any submissions for which the Guest Editors have competing interests is handled by another Editorial Board Member who has no competing interests.