Research progress on neuroimmune interactions in diabetic retinopathy

Authors:Zhang Danlei, Hou Shengping

Corresponding author: Hou Shengping, Email: sphou828@163.com

Published:2026-09-10

DOI:10.3760/cma.j.cn115989-20260422-00186

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ABSTRACT 

Diabetic retinopathy (DR) is a common microvascular complication of diabetes and one of the main blinding eye diseases. Recent studies have shown that retinal neurodegenerative changes and chronic low-grade inflammation can occur in the early stage of DR and participate in the progression of the disease. The two-way signal communication between nerve cells and immune cells may be an important part of the early pathological process of DR. This article summarizes the physiological basis of neuroimmune interactions in the retina, focusing on the related mechanisms of immune response-mediated nerve injury and nerve cell regulation of immune response. In terms of mechanism, existing studies have shown that microglial activation and immunometabolic reprogramming, Müller cell dysfunction and related inflammatory signaling pathways are all related to neuroinflammation and neurodegenerative changes. Signaling axes such as CX3CL1-CX3CR1 and CD200-CD200R are involved in maintaining microglial homeostasis and regulating inflammatory responses. In addition, this paper also summarizes the candidate biomarkers reflecting neuroimmune abnormalities and related intervention strategies, in order to provide reference for understanding the early pathological changes of DR and exploring new prevention and treatment approaches.

KEYWORDS：

Diabetic retinopathy;Neurodegeneration;Inflammation;Microglia;Neuroimmune interaction

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All articles published represent the opinions of the authors, and do not reflect the official policy of the Chinese Medical Association or the Editorial Board, unless this is clearly specified.

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Authors Info & Affiliations 

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Figures & Tables

Figure 1 Mechanism of neuroimmune interaction in DR Continuous high glucose and the metabolic disorders it causes can lead to dysfunction of retinal neurons, microglia, Müller cells, vascular endothelial cells and inner layer BRB, and mediate the mutual promotion of neurodegenerative changes, chronic low-grade inflammation, BRB damage and microangiopathy through multiple intercellular signals. Blue solid arrows indicate the role of maintaining homeostasis or inhibiting inflammation; red solid arrows indicate the role of promoting inflammation or tissue damage; red dotted arrows indicate that there is currently limited direct causal evidence for the relevant mechanism in early DR.

DR: diabetic retinopathy;BRB: Blood-retinal barrier; CX3CL1: C-X3-C motif chemokine ligand 1; CX3CR1: C-X3-C motif chemokine receptor 1; CD200: Cluster of Differentiation 200; CD200R: CD200 receptor; LysoPS： Lysophosphatidylserine; GPR34： G protein-coupled receptor 34; IL-1β： interleukin-1β; TNF-α： Tumor necrosis factor alpha; ROS： Reactive oxygen species; C1q： Complement component 1q; C3： Complement component 3; CR3： Complement receptor 3; CSF1： Colony stimulating factor 1; CSF1R： Colony stimulating factor 1 receptor; CD40： differentiation antigen cluster 40; ATP： Adenosine triphosphate; P2X7： P2X purinergic receptor 7; VEGF： vascular endothelial growth factor

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