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 (668 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
The movement of cells or organisms toward or away from a substance in response to its concentration gradient.
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: Haptotaxis.
Where it fits in the MeSH classification
- Broader topics
- Taxis Response; Cell Movement
- Narrower topics
- Chemotaxis, Leukocyte
- See also
- Chemoreceptor Cells; Chemotactic Factors
Research landscape
PubMed indexes 31,819 records tagged with the MeSH heading “Chemotaxis” (counts retrieved 2026-10-29). 1,963 of them (6.2%) were published from 2020 onward, and the busiest period so far is through 1999 with 13,191 records.
Reviews account for 3,157 records (9.9%) and meta-analyses for 4. Randomized controlled trials number 98 (0.3%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 13,191 |
| 2000-2009 | 9,238 |
| 2010-2019 | 7,427 |
| 2020 onward | 1,963 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 3,157 | 9.9% |
| Meta-analyses | 4 | 0.0% |
| Randomized controlled trials | 98 | 0.3% |
Method: PubMed query "Chemotaxis"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in molecular biology
Molecular biology establishes mechanisms through controlled experiments, often in simplified systems such as purified proteins, cultured cells or model organisms. Such work can show what is possible in a defined system, but whether a pathway matters in a whole organism or in human disease needs further evidence. Check the experimental system, whether findings were reproduced by independent groups, and whether the authors tested the mechanism directly or inferred it from correlation.
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 |
|---|---|---|---|---|
| Sensing of autoinducer-2 by functionally distinct receptors in prokaryotes | 2020 | Research article Design not recorded in structured metadata | 155 | cc by PMID 33097715 · DOI · PMC7584622 |
| Targeting myeloid chemotaxis to reverse prostate cancer therapy resistance | 2023 | Research article Design not recorded in structured metadata | 129 | cc by PMID 37844613 · DOI · PMC10686834 |
| Circadian clocks guide dendritic cells into skin lymphatics | 2021 | Research article Design not recorded in structured metadata | 109 | cc by PMID 34663979 · DOI · PMC8553624 |
| cPLA2α targeting to exosomes connects nuclear deformation to LTB4-signaling during neutrophil chemotaxis | 2026 | Research article Design not recorded in structured metadata | 5 | cc by PMID 41719396 · DOI · PMC12922757 |
Sensing of autoinducer-2 by functionally distinct receptors in prokaryotes [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Autoinducer-2 (AI-2) is a quorum sensing signal that mediates communication within and between many bacterial species.
- Closing excerpt
- Our results support the idea that AI-2 serves as a widely used signaling molecule in the coordination of cell behavior among prokaryotic species.
- 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 (159 words)
Autoinducer-2 (AI-2) is a quorum sensing signal that mediates communication within and between many bacterial species. However, its known receptors (LuxP and LsrB families) are not found in all the bacteria capable of responding to this signaling molecule. Here, we identify a third type of AI-2 receptor, consisting of a dCACHE domain. AI-2 binds to the dCACHE domain of chemoreceptors PctA and TlpQ of Pseudomonas aeruginosa, thus inducing chemotaxis and biofilm formation. Boron-free AI-2 is the preferred ligand for PctA and TlpQ. AI-2 also binds to the dCACHE domains of histidine kinase KinD from Bacillus subtilis and diguanylate cyclase rpHK1S-Z16 from Rhodopseudomonas palustris, enhancing their enzymatic activities. dCACHE domains (especially those belonging to a subfamily that includes the AI-2 receptors identified in the present work) are present in a large number of bacterial and archaeal proteins. Our results support the idea that AI-2 serves as a widely used signaling molecule in the coordination of cell behavior among prokaryotic species.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 33097715 · DOI · PMC7584622
Targeting myeloid chemotaxis to reverse prostate cancer therapy resistance [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Inflammation is a hallmark of cancer1.
- Closing excerpt
- Targeting myeloid chemotaxis merits broader evaluation in other cancers.
- 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 (214 words)
Inflammation is a hallmark of cancer1. In patients with cancer, peripheral blood myeloid expansion, indicated by a high neutrophil-to-lymphocyte ratio, associates with shorter survival and treatment resistance across malignancies and therapeutic modalities2-5. Whether myeloid inflammation drives progression of prostate cancer in humans remain unclear. Here we show that inhibition of myeloid chemotaxis can reduce tumour-elicited myeloid inflammation and reverse therapy resistance in a subset of patients with metastatic castration-resistant prostate cancer (CRPC). We show that a higher blood neutrophil-to-lymphocyte ratio reflects tumour myeloid infiltration and tumour expression of senescence-associated mRNA species, including those that encode myeloid-chemoattracting CXCR2 ligands. To determine whether myeloid cells fuel resistance to androgen receptor signalling inhibitors, and whether inhibiting CXCR2 to block myeloid chemotaxis reverses this, we conducted an investigator-initiated, proof-of-concept clinical trial of a CXCR2 inhibitor (AZD5069) plus enzalutamide in patients with metastatic CRPC that is resistant to androgen receptor signalling inhibitors. This combination was well tolerated without dose-limiting toxicity and it decreased circulating neutrophil levels, reduced intratumour CD11b+HLA-DRloCD15+CD14- myeloid cell infiltration and imparted durable clinical benefit with biochemical and radiological responses in a subset of patients with metastatic CRPC. This study provides clinical evidence that senescence-associated myeloid inflammation can fuel metastatic CRPC progression and resistance to androgen receptor blockade. Targeting myeloid chemotaxis merits broader evaluation in other cancers.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 37844613 · DOI · PMC10686834
Circadian clocks guide dendritic cells into skin lymphatics [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Migration of leukocytes from the skin to lymph nodes (LNs) via afferent lymphatic vessels (LVs) is pivotal for adaptive immune responses1,2.
- Closing excerpt
- These observations indicate that circadian clocks control the infiltration of DCs into skin lymphatics, a process that is essential for many adaptive immune responses and relevant for vaccination and immunotherapies.
- 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 (151 words)
Migration of leukocytes from the skin to lymph nodes (LNs) via afferent lymphatic vessels (LVs) is pivotal for adaptive immune responses1,2. Circadian rhythms have emerged as important regulators of leukocyte trafficking to LNs via the blood3,4. Here, we demonstrate that dendritic cells (DCs) have a circadian migration pattern into LVs, which peaks during the rest phase in mice. This migration pattern is determined by rhythmic gradients in the expression of the chemokine CCL21 and of adhesion molecules in both mice and humans. Chronopharmacological targeting of the involved factors abrogates circadian migration of DCs. We identify cell-intrinsic circadian oscillations in skin lymphatic endothelial cells (LECs) and DCs that cogovern these rhythms, as their genetic disruption in either cell type ablates circadian trafficking. These observations indicate that circadian clocks control the infiltration of DCs into skin lymphatics, a process that is essential for many adaptive immune responses and relevant for vaccination and immunotherapies.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 34663979 · DOI · PMC8553624
cPLA2α targeting to exosomes connects nuclear deformation to LTB4-signaling during neutrophil chemotaxis [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Efficient neutrophil chemotaxis requires the integration of mechanical forces and lipid-mediated signaling.
- Closing excerpt
- These findings uncover a cPLA2α-dependent mechanochemical axis linking nuclear architecture to chemotactic efficiency and offer alternative strategies to modulate inflammatory responses.
- 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 (144 words)
Efficient neutrophil chemotaxis requires the integration of mechanical forces and lipid-mediated signaling. While the signaling lipid leukotriene B4 (LTB4) reinforces cellular polarity, how mechanical cues regulate its production remains unclear. We now show that cytosolic phospholipase A2α (cPLA2α), which is essential for the synthesis of LTB4, functions as a nuclear curvosensor. cPLA2α responds to nuclear squeezing by localizing to ceramide-rich inner nuclear membrane microdomains and incorporating onto the exofacial surface of nuclear envelope-derived exosomes. This unique topology enables localized LTB4 synthesis, which synchronizes calcium spikes, promotes myosin light chain II phosphorylation, and sustains polarity and directional persistence after constriction. In neutrophils passing through tight spaces, cPLA2α activity drives the chemotactic response to nuclear squeezing by promoting exosomal LTB4 production and persistence after constriction. These findings uncover a cPLA2α-dependent mechanochemical axis linking nuclear architecture to chemotactic efficiency and offer alternative strategies to modulate inflammatory responses.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41719396 · DOI · PMC12922757
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 Chemotaxis in cancer [5]
- Research article Chemokine: receptor structure, interactions, and antagonism [6]
- Research article Vascular adhesion molecules in atherosclerosis [7]
- Research article Bacterial chemoreceptors: high-performance signaling in networked arrays [8]
- Research article PECAM-1: a multi-functional molecule in inflammation and vascular biology [9]
- Research article Interstitial leukocyte migration and immune function [10]
References
- Zhang L, Li S, Liu X, Wang Z, Jiang M, Wang R, et al.. Sensing of autoinducer-2 by functionally distinct receptors in prokaryotes. . 2020. PMID 33097715 · DOI · PMC7584622
- Guo C, Sharp A, Gurel B, Crespo M, Figueiredo I, Jain S, et al.. Targeting myeloid chemotaxis to reverse prostate cancer therapy resistance. . 2023. PMID 37844613 · DOI · PMC10686834
- Holtkamp SJ, Ince LM, Barnoud C, Schmitt MT, Sinturel F, Pilorz V, et al.. Circadian clocks guide dendritic cells into skin lymphatics. . 2021. PMID 34663979 · DOI · PMC8553624
- Arya SB, Jordan-Javed F, Loesel K, Choi Y, Collie SP, Hein LE, et al.. cPLA2α targeting to exosomes connects nuclear deformation to LTB4-signaling during neutrophil chemotaxis. . 2026. PMID 41719396 · DOI · PMC12922757
- Roussos ET, Condeelis JS, Patsialou A. Chemotaxis in cancer. Nat Rev Cancer. 2011. PMID 21779009 · DOI · PMC4030706
- Allen SJ, Crown SE, Handel TM. Chemokine: receptor structure, interactions, and antagonism. Annu Rev Immunol. 2007. PMID 17291188 · DOI
- Galkina E, Ley K. Vascular adhesion molecules in atherosclerosis. Arterioscler Thromb Vasc Biol. 2007. PMID 17673705 · DOI
- Hazelbauer GL, Falke JJ, Parkinson JS. Bacterial chemoreceptors: high-performance signaling in networked arrays. Trends Biochem Sci. 2008. PMID 18165013 · DOI · PMC2890293
- Woodfin A, Voisin MB, Nourshargh S. PECAM-1: a multi-functional molecule in inflammation and vascular biology. Arterioscler Thromb Vasc Biol. 2007. PMID 17872453 · DOI
- Friedl P, Weigelin B. Interstitial leukocyte migration and immune function. Nat Immunol. 2008. PMID 18711433 · 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 2026-10-29.
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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.