ArticleVascular biology (Bristol, England)2023
Intercellular adhesion molecule 2 regulates diapedesis hotspots by allowing neutrophil crawling against the direction of flow.
Article in Vascular biology (Bristol, England), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 5 citations in OpenAlex.
- Spleen-derived circulating intercellular adhesion molecule 2 promotes osteosclerosis in chronic myelofibrosis.Bone research · 2026Article
- Identification and Analysis of Remimazolam's Potential Therapeutic Mechanisms in Murine Sepsis-Associated Encephalopathy via Transcriptomic Analysis.Journal of inflammation research · 2026Article
- Mechanisms That Prevent Vascular Leakage During Leukocyte Extravasation.Acta physiologica (Oxford, England) · 2025Review
- Nanoscopy reveals integrin clustering reliant on kindlin-3 but not talin-1.Cell communication and signaling : CCS · 2025Article
- Assessment of NK cytotoxicity and interactions with porcine endothelial cells by live-cell imaging in 2D static and 3D microfluidic systems.Scientific reports · 2024Article
- Phenotypic and Functional Diversity of Neutrophils in Gut Inflammation and Cancer.The American journal of pathology · 2024Review
- Not all (cells) who wander are lost: Upstream migration as a pervasive mode of amoeboid cell motility.Frontiers in cell and developmental biology · 2023Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intercellular adhesion molecules (ICAMs) are cell surface proteins that play a crucial role in the body's immune response and inflammatory processes. ICAM1 and ICAM2 are two ICAM family members expressed on the surface of various cell types, including endothelial cells. They mediate the interaction between immune cells and endothelial cells, which are critical for the trafficking of leukocytes across the blood vessel wall during inflammation. Although ICAM1 plays a prominent role in the leukocyte extravasation cascade, it is less clear if ICAM2 strengthens ICAM1 function or has a separate function in the cascade. With CRISPR-)Cas9 technology, endothelial cells were depleted for ICAM1,ICAM2, or both, and we found that neutrophils favored ICAM1 over ICAM2 to adhere to. However, the absence of only ICAM2 resulted in neutrophils that were unable to find the transmigration hotspot, i.e. the preferred exit site. Moreover, we found that ICAM2 deficiency prevented neutrophils to migrate against the flow. Due to this deficiency, we concluded that ICAM2 helps neutrophils find the preferred exit sites and thereby contributes to efficient leukocyte extravasation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.