# Comprehensive immunological profiling of acute ischemic stroke during mechanical thrombectomy: myeloid cell activation and molecular signatures in blood and thrombus

**Authors:** Wirginia Krzyściak, Tadeusz Popiela

PMC · DOI: 10.3389/fstro.2026.1731953 · Frontiers in Stroke · 2026-02-12

## TL;DR

This study aims to understand immune responses in stroke patients by analyzing blood and thrombus samples during mechanical thrombectomy.

## Contribution

The study introduces a multi-compartment immunological and molecular profiling approach in acute ischemic stroke.

## Key findings

- Immune profiles from arterial blood, peripheral blood, and thrombus will be compared.
- Associations between immune markers and clinical outcomes will be evaluated.
- Integration of immune and clinical data may reveal predictive biomarkers for stroke recovery.

## Abstract

Acute ischemic stroke (AIS) induces a complex local and systemic inflammatory response; however, most studies rely solely on peripheral blood, providing an incomplete view of immune activity at the occlusion site and within the thrombus.

To characterize immune activation and transcriptomic signatures of myeloid cells across three compartments—arterial blood at the occlusion site, peripheral blood, and thrombus—and to evaluate their associations with radiological and clinical outcomes following mechanical thrombectomy.

This prospective, single-center study will include AIS patients treated with mechanical thrombectomy. Matched arterial, peripheral, and thrombus samples will undergo spectral flow cytometry, cytokine profiling, cell-free DNA (cfDNA) quantification, microscopy, and RNA sequencing. Immune and molecular readouts will be correlated with clinical scores (NIHSS, mRS), imaging markers (e.g., hyperdense middle cerebral artery sign [HMCAS]), and procedural outcomes (TICI score, number of passes).

Integrating local and systemic immune profiles with clinical and radiological parameters may identify biomarkers predictive of thrombectomy efficacy and functional recovery, thereby supporting precision-medicine approaches in AIS.

www.ClinicalTrials.gov

## Full-text entities

- **Genes:** RIPK1 (receptor interacting serine/threonine kinase 1) [NCBI Gene 8737] {aka AIEFL, IMD57, RIP, RIP-1, RIP1}, CEACAM8 (CEA cell adhesion molecule 8) [NCBI Gene 1088] {aka CD66b, CD67, CGM6, NCA-95}, ITGAM (integrin subunit alpha M) [NCBI Gene 3684] {aka CD11B, CR3A, HNA-4, MAC-1, MAC1A, MO1A}, PLAT (plasminogen activator, tissue type) [NCBI Gene 5327] {aka T-PA, TPA}, MIF (macrophage migration inhibitory factor) [NCBI Gene 4282] {aka GIF, GLIF, MMIF}, CD68 (CD68 molecule) [NCBI Gene 968] {aka GP110, LAMP4, SCARD1}, ANXA5 (annexin A5) [NCBI Gene 308] {aka ANX5, CPB-I, ENX2, HEL-S-7, PP4, RPRGL3}
- **Diseases:** atherosclerotic (MESH:D050197), occlusion (MESH:D001157), death (MESH:D003643), Thrombotic (MESH:D013927), Ischemic Stroke (MESH:D002544), infection (MESH:D007239), wall (MESH:D056988), Infarct (MESH:D007238), bruising (MESH:D003288), tissue damage (MESH:D017695), MT (MESH:D041781), vascular occlusion (MESH:D008641), pain (MESH:D010146), NIHSS (MESH:C538175), hematoma (MESH:D006406), cardiogenic thrombi (MESH:D013575), inflammation (MESH:D007249), Lymphopenia (MESH:D008231), ischemic (MESH:D002545), large-vessel occlusion (MESH:C536223), Stroke (MESH:D020521), bleeding (MESH:D006470), NET (MESH:C536657), hemolysis (MESH:D006461), AIS (MESH:D000083242)
- **Chemicals:** H&amp;E (MESH:D006371), IVT (-), formalin (MESH:D005557), PI (MESH:D010716), Trypan Blue (MESH:D014343), paraffin (MESH:D010232), EDTA (MESH:D004492)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12935871/full.md

## References

34 references — full list in the complete paper: https://tomesphere.com/paper/PMC12935871/full.md

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Source: https://tomesphere.com/paper/PMC12935871