What is the clinical evidence from this study?

Population: Atherosclerosis. Intervention: Endothelial Elavl1 deletion vs. Wild-type. Primary outcome: CD8 T-cell accumulation at plaques (≈70% reduction).

What question did this study set out to answer?

Determine whether endothelial Elavl1 regulates gene expression programs and CD8 T-cell activation and persistence within atherosclerotic lesions.

April 11, 2026Arteriosclerosis Thrombosis and Vascular BiologyOpen Access

Endothelial Elavl1 Is Required for CD8 T-Cell Persistence in Atherosclerosis

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Key result

Endothelial Elavl1 suppression limits CD8 T-cell persistence in atherosclerosis via checkpoint-like regulation.

≈70% reduction

Why the study?

It is unknown whether endothelial cells regulate CD8 T-cell activation and persistence in atherosclerosis through posttranscriptional control mechanisms involving Elavl1.

Population

Endothelial cell-knockout mice and in vitro endothelial cell models

Comparison

Deletion of endothelial Elavl1 vs wild-type control

Design

Preclinical experimental study

Authors

SNSarah-Anne E. NicholasAnna Needs Neuroblastoma Answers SHStephen B. HelmingAnna Needs Neuroblastoma Answers AMAntoine MénoretUniversity of Connecticut

Discussion

Member takes

Implication

Endothelial Elavl1 acts as a local immune checkpoint-like regulator, and its suppression reduces CD8 T-cell persistence in atherosclerosis.

Key Points

Determine whether endothelial Elavl1 regulates gene expression programs and CD8 T-cell activation and persistence within atherosclerotic lesions.
Generated endothelial cell-knockout mice to evaluate the impact of endothelial Elavl1 deficiency on immune cell activity and vascular gene expression during atherosclerosis.
Assessed mRNA alternative splicing motifs, 5' untranslated region ribosomal associations, and in vitro antigen-dependent CD8 T-cell persistence with wild-type myeloid antigen-presenting cells.
Endothelial Elavl1 deletion amplified atherogenic gene expression programs and decreased CD8 T-cell accumulation in atherosclerotic plaques by approximately 70% without altering initial cell recruitment.
Elavl1-deficient endothelial cells in vitro directly suppressed antigen-dependent CD8 T-cell persistence, even when co-cultured with wild-type myeloid antigen-presenting cells and cognate antigen.

Structured PICO

Population

Endothelial cell-knockout mice and in vitro endothelial cell models

Intervention

Deletion of endothelial Elavl1 (ELAV-like RNA-binding protein 1)

Comparator

Wild-type/control

Outcome

CD8 T-cell accumulation and persistence at atherosclerotic plaquessurrogate

Main Result

Effect estimate: ≈70% reduction

Endothelial Elavl1 acts as a local immune checkpoint-like regulator, and its suppression reduces CD8 T-cell persistence in atherosclerosis.

Cite This Study

Nicholas et al. (2026) studied Atherosclerosis. Endothelial Elavl1 deletion vs. Wild-type was evaluated on CD8 T-cell accumulation at plaques (≈70% reduction). Endothelial Elavl1 deletion reduced CD8 T-cell accumulation at atherosclerotic plaques by approximately 70% without affecting recruitment, indicating impaired persistence.

synapsesocial.com/papers/69d9e67a78050d08c1b76d50 https://doi.org/10.1161/atvbaha.125.323674

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Implication

Endothelial Elavl1 acts as a local immune checkpoint-like regulator, and its suppression reduces CD8 T-cell persistence in atherosclerosis.

Endothelial Elavl1 Is Required for CD8 T-Cell Persistence in Atherosclerosis

Discussion

Member takes

Implication

Key Points

Structured PICO

Main Result

Cite This Study

Endothelial Elavl1 Is Required for CD8 T-Cell Persistence in Atherosclerosis

Discussion

Member takes

Implication

Key Points

Structured PICO

Main Result

Cite This Study

Also Consider

Also Consider