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Inhibition of LCP2 in T cells alleviated apoptosis and oxidative stress via PD-1/PD-L1 in diabetic retinopathy

  • 0Department of Ophthalmology, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, China; Department of Ophthalmology, Aier Eye Hospital of Wuhan University, Wuhan 430060, Hubei Province, China.
International Immunopharmacology +

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July 23, 2025

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July 23, 2025

View abstract on PubMed

Summary

This summary is machine-generated.

Lymphocyte cytosolic protein 2 (LCP2) is a key platelet biomarker in diabetic retinopathy (DR). Targeting the LCP2-PD-1/PD-L1 pathway may offer a novel treatment for DR by reducing inflammation and cell death.

Area Of Science

  • Ophthalmology
  • Immunology
  • Molecular Biology

Background

  • Diabetic retinopathy (DR) is a leading cause of vision loss.
  • Platelet activation and immune dysregulation are implicated in DR pathogenesis.
  • The role of lymphocyte cytosolic protein 2 (LCP2) and the PD-1/PD-L1 pathway in DR remains unclear.

Purpose Of The Study

  • To identify platelet-related biomarkers for DR.
  • To elucidate the role of LCP2 and the PD-1/PD-L1 pathway in DR.
  • To investigate potential therapeutic targets for DR.

Main Methods

  • Bioinformatics analysis of DR datasets to identify platelet-related genes.
  • Validation using qRT-PCR in diabetic rat models and high-glucose treated cells.
  • In vivo studies with PD-1/PD-L1 inhibitors and LCP2 knockdown in diabetic rats.
  • In vitro co-culture models of T cells and retinal pigment epithelial cells (RPECs).

Main Results

  • Nine core platelet-related genes were identified, with LCP2 being significantly upregulated in DR models.
  • Increased LCP2 and PD-1/PD-L1 expression correlated with retinal injury, inflammation, oxidative stress, and apoptosis.
  • Inhibition of LCP2 or PD-1/PD-L1, especially in combination, ameliorated DR pathology.
  • LCP2 knockdown reversed high-glucose-induced RPEC damage and inflammation.

Conclusions

  • LCP2 is a critical platelet-related biomarker in DR.
  • LCP2 exacerbates DR by activating the PD-1/PD-L1 axis, promoting inflammation and apoptosis.
  • Targeting the LCP2-PD-1/PD-L1 axis presents a promising therapeutic strategy for DR.

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