Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (678 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A cell-surface ligand involved in leukocyte adhesion and inflammation. Its production is induced by gamma-interferon and it is required for neutrophil migration into inflamed tissue.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Intercellular Adhesion Molecule 1; CD54 Antigen; Antigen, CD54; Antigens, CD54; CD54 Antigens; ICAM-1.
Where it fits in the MeSH classification
- Broader topics
- Cell Adhesion Molecules
Research landscape
PubMed indexes 19,370 records tagged with the MeSH heading “Intercellular Adhesion Molecule-1” (counts retrieved 2026-10-31). 1,654 of them (8.5%) were published from 2020 onward, and the busiest period so far is 2000-2009 with 7,198 records.
Reviews account for 705 records (3.6%) and meta-analyses for 60. Randomized controlled trials number 507 (2.6%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 5,380 |
| 2000-2009 | 7,198 |
| 2010-2019 | 5,138 |
| 2020 onward | 1,654 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 705 | 3.6% |
| Meta-analyses | 60 | 0.3% |
| Randomized controlled trials | 507 | 2.6% |
Method: PubMed query "Intercellular Adhesion Molecule-1"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in drugs and chemicals
Studies of a chemical or drug can answer very different questions: what it is and how it behaves in cells and animals, how the body handles it, and whether it changes outcomes in people. Laboratory and animal findings often do not carry over to patients, and observational studies of exposures are confounded by who uses a substance and why. Nothing on this page is a recommendation to use, avoid, start or stop any substance or medicine; talk to a qualified clinician or pharmacist about your own situation. Check the dose, the species, the comparison group and whether a patient-relevant outcome was measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| LFA-1 in T Cell Migration and Differentiation | 2018 | Review article Design not recorded in structured metadata | 225 | cc by PMID 29774029 · DOI · PMC5943560 |
| ICAM1 initiates CTC cluster formation and trans-endothelial migration in lung metastasis of breast cancer | 2021 | Research article Design not recorded in structured metadata | 204 | cc by PMID 34381029 · DOI · PMC8358026 |
| Tumour-derived Interleukin 35 promotes pancreatic ductal adenocarcinoma cell extravasation and metastasis by inducing ICAM1 expression | 2017 | Research article Design not recorded in structured metadata | 103 | cc by PMID 28102193 · DOI · PMC5253665 |
| ICAM-1 identifies preadipocytes and restricts white adipogenesis by adhering immune cells | 2026 | Research article Design not recorded in structured metadata | 2 | cc by PMID 40813463 · DOI · PMC12881632 |
LFA-1 in T Cell Migration and Differentiation [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Maintenance of homeostatic immune surveillance and development of effective adaptive immune responses require precise regulation of spatial and temporal lymphocyte trafficking throughout the body to ensure pathogen clearance and memory generation.
- Closing excerpt
- Here, we summarize the roles of LFA-1 and ongoing studies to better understand its functions and regulation.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (215 words)
Maintenance of homeostatic immune surveillance and development of effective adaptive immune responses require precise regulation of spatial and temporal lymphocyte trafficking throughout the body to ensure pathogen clearance and memory generation. Dysregulation of lymphocyte activation and migration can lead to impaired adaptive immunity, recurrent infections, and an array of autoimmune diseases and chronic inflammation. Central to the recruitment of T cells, integrins are cell surface receptors that regulate adhesion, signal transduction, and migration. With 24 integrin pairs having been discovered to date, integrins are defined not only by the composition of the heterodimeric pair but by cell-type specific expression and their ligands. Furthermore, integrins not only facilitate adhesion but also induce intracellular signaling and have recently been uncovered as mechanosensors providing additional complexity to the signaling pathways. Among several leukocyte-specific integrins, lymphocyte function-associated antigen-1 (LFA-1 or αLβ2; CD11a/CD18) is a key T cell integrin, which plays a major role in regulating T cell activation and migration. Adhesion to LFA-1's ligand, intracellular adhesion receptor 1 (ICAM-1) facilitates firm endothelium adhesion, prolonged contact with antigen-presenting cells, and binding to target cells for killing. While the downstream signaling pathways utilized by LFA-1 are vastly conserved they allow for highly disparate responses. Here, we summarize the roles of LFA-1 and ongoing studies to better understand its functions and regulation.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 29774029 · DOI · PMC5943560
ICAM1 initiates CTC cluster formation and trans-endothelial migration in lung metastasis of breast cancer [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Circulating tumor cell (CTC) clusters mediate metastasis at a higher efficiency and are associated with lower overall survival in breast cancer compared to single cells.
- Closing excerpt
- Therefore, ICAM1 can serve as a novel therapeutic target for metastasis initiation of TNBC.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (154 words)
Circulating tumor cell (CTC) clusters mediate metastasis at a higher efficiency and are associated with lower overall survival in breast cancer compared to single cells. Combining single-cell RNA sequencing and protein analyses, here we report the profiles of primary tumor cells and lung metastases of triple-negative breast cancer (TNBC). ICAM1 expression increases by 200-fold in the lung metastases of three TNBC patient-derived xenografts (PDXs). Depletion of ICAM1 abrogates lung colonization of TNBC cells by inhibiting homotypic tumor cell-tumor cell cluster formation. Machine learning-based algorithms and mutagenesis analyses identify ICAM1 regions responsible for homophilic ICAM1-ICAM1 interactions, thereby directing homotypic tumor cell clustering, as well as heterotypic tumor-endothelial adhesion for trans-endothelial migration. Moreover, ICAM1 promotes metastasis by activating cellular pathways related to cell cycle and stemness. Finally, blocking ICAM1 interactions significantly inhibits CTC cluster formation, tumor cell transendothelial migration, and lung metastasis. Therefore, ICAM1 can serve as a novel therapeutic target for metastasis initiation of TNBC.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 34381029 · DOI · PMC8358026
Tumour-derived Interleukin 35 promotes pancreatic ductal adenocarcinoma cell extravasation and metastasis by inducing ICAM1 expression [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Interleukin 35 (IL-35) is a novel member of the IL-12 family, consisting of an EBV-induced gene 3 (EBI3) subunit and a P35 subunit.
- Closing excerpt
- Together, our results indicate additional functions of IL-35 in promoting PDAC metastasis through mediating ICAM1 expression.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (146 words)
Interleukin 35 (IL-35) is a novel member of the IL-12 family, consisting of an EBV-induced gene 3 (EBI3) subunit and a P35 subunit. IL-35 is an immune-suppressive cytokine mainly produced by regulatory T cells. However, the role of IL-35 in cancer metastasis and progression is not well understood. Here we demonstrate that IL-35 is overexpressed in human pancreatic ductal adenocarcinoma (PDAC) tissues, and that IL-35 overexpression is associated with poor prognosis in PDAC patients. IL-35 has critical roles in PDAC cell extravasation and metastasis by facilitating the adhesion to endothelial cells and transendothelial extravasation. Mechanistically, IL-35 promotes ICAM1 overexpression through a GP130-STAT1 signalling pathway, which facilitates endothelial adhesion and transendothelial migration via an ICAM1-fibrinogen-ICAM1 bridge. In an orthotopic xenograft model, IL-35 promotes spontaneous pancreatic cancer metastasis in an ICAM1-dependent manner. Together, our results indicate additional functions of IL-35 in promoting PDAC metastasis through mediating ICAM1 expression.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 28102193 · DOI · PMC5253665
ICAM-1 identifies preadipocytes and restricts white adipogenesis by adhering immune cells [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Adipose stem cell hierarchy was delineated by scRNA-seq analysis, revealing that ICAM-1, a glycoprotein that mediates cell-cell interaction, is a preadipocyte marker.
- Closing excerpt
- Thus, our study shows that ICAM-1 marks preadipocytes and curbs adipogenesis by facilitating adhesion between preadipocytes and immune cells.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (163 words)
Adipose stem cell hierarchy was delineated by scRNA-seq analysis, revealing that ICAM-1, a glycoprotein that mediates cell-cell interaction, is a preadipocyte marker. However, the cellular and molecular mechanisms of how ICAM-1+ preadipocytes contribute to adipose tissue homeostasis in vivo remain unclear. To address this, Icam1+/CreERT2 mice were generated, and it was demonstrated that ICAM-1-expressing progenitors actively participated in developing and remodeling white adipose tissue. Under a high-fat diet, both proliferation and adipogenic differentiation of ICAM-1+ preadipocytes increased significantly. Interestingly, ICAM-1 plays a critical role in maintaining the interaction between preadipocytes and immune cells, acting as a checkpoint on white adipogenesis. Mice lacking ICAM-1 specifically in stromal cells exhibited worsened hyperplastic obesity, showing heightened fatty acid synthesis and lipid storage in adipose tissue, and the related insulin resistance. In human adipose tissue, ICAM-1 also marked committed preadipocytes and mediated adhesion between preadipocytes and immune cells. Thus, our study shows that ICAM-1 marks preadipocytes and curbs adipogenesis by facilitating adhesion between preadipocytes and immune cells.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40813463 · DOI · PMC12881632
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Transcriptional regulation of endothelial cell adhesion molecules: NF-kappa B and cytokine-inducible enhancers [5]
- Research article ICAM-1: A master regulator of cellular responses in inflammation, injury resolution, and tumorigenesis [6]
- Research article Intercellular adhesion molecule-1 [7]
- Research article ICAM-1 signaling in endothelial cells [8]
- Research article Intercellular adhesion molecule-1 (ICAM-1) expression and cell signaling cascades [9]
- Research article Regulation of intercellular adhesion molecule-1 (CD54) gene expression [10]
References
- Walling BL, Kim M. LFA-1 in T Cell Migration and Differentiation. . 2018. PMID 29774029 · DOI · PMC5943560
- Taftaf R, Liu X, Singh S, Jia Y, Dashzeveg NK, Hoffmann AD, et al.. ICAM1 initiates CTC cluster formation and trans-endothelial migration in lung metastasis of breast cancer. . 2021. PMID 34381029 · DOI · PMC8358026
- Huang C, Li N, Li Z, Chang A, Chen Y, Zhao T, et al.. Tumour-derived Interleukin 35 promotes pancreatic ductal adenocarcinoma cell extravasation and metastasis by inducing ICAM1 expression. . 2017. PMID 28102193 · DOI · PMC5253665
- Zheng C, Ye J, Yang Q, Liu K, Chen C, Cao J, et al.. ICAM-1 identifies preadipocytes and restricts white adipogenesis by adhering immune cells. . 2026. PMID 40813463 · DOI · PMC12881632
- Collins T, Read MA, Neish AS, Whitley MZ, Thanos D, Maniatis T. Transcriptional regulation of endothelial cell adhesion molecules: NF-kappa B and cytokine-inducible enhancers. FASEB J. 1995. PMID 7542214 · DOI
- Bui TM, Wiesolek HL, Sumagin R. ICAM-1: A master regulator of cellular responses in inflammation, injury resolution, and tumorigenesis. J Leukoc Biol. 2020. PMID 32182390 · DOI · PMC7977775
- van de Stolpe A, van der Saag PT. Intercellular adhesion molecule-1. J Mol Med (Berl). 1996. PMID 8834767 · DOI
- Lawson C, Wolf S. ICAM-1 signaling in endothelial cells. Pharmacol Rep. 2009. PMID 19307690 · DOI
- Hubbard AK, Rothlein R. Intercellular adhesion molecule-1 (ICAM-1) expression and cell signaling cascades. Free Radic Biol Med. 2000. PMID 10924857 · DOI
- Roebuck KA, Finnegan A. Regulation of intercellular adhesion molecule-1 (CD54) gene expression. J Leukoc Biol. 1999. PMID 10614768 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.