GO:2000503 positive regulation of natural killer cell chemotaxis: Immune Recruitment Pathway, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:2000503 describes any process that increases the frequency, rate or extent of natural killer (NK) cell chemotaxis, the directed migration of NK cells along chemical gradients.
• Monocyte chemotactic proteins MCP-1, MCP-2 and MCP-3 directly induce NK cell migration, establishing chemokine-driven NK recruitment as a core positive regulatory mechanism.
• NK cells themselves produce T cell-recruiting chemokines in response to antibody-coated tumor cells, linking positive regulation of NK chemotaxis to broader immune cell recruitment loops.
• KCa3.1 potassium channels regulate tumor infiltration of functionally competent NK cells, showing that ion channel activity can gate NK cell chemotaxis into tumors.
• IL-1R8 expression in diffuse large B-cell lymphoma regulates NK cell recruitment and influences patient prognosis, connecting this GO term to clinical outcome.
• Experimental dissection of GO:2000503 uses chemotaxis assays, cytokine/chemokine profiling, CRISPR knockout and knock-in models, and bioinformatic immune deconvolution [1,3,8].
Description
Positive regulation of natural killer cell chemotaxis (GO:2000503) is the biological process that activates or increases the frequency, rate or extent of NK cell chemotaxis, the directed movement of NK cells along chemical gradients. NK cells are innate lymphoid effectors that must physically reach infected or transformed tissues to exert cytotoxicity, so the positive regulation of their migration is a prerequisite for effective immune surveillance. The term sits within the broader ontology of leukocyte chemotaxis and is defined by the QuickGO resource as any process that activates or increases NK cell chemotaxis. Because NK cell infiltration into tumors correlates with prognosis in several malignancies, understanding what positively regulates this migration has direct translational value [6,7]. Chemokines such as monocyte chemotactic protein-1 (MCP-1/CCL2), MCP-2 (CCL8) and MCP-3 (CCL7) were among the first factors shown to induce NK cell migration in vitro, providing the founding experimental evidence for this process. Subsequent work demonstrated that NK cells can themselves secrete T cell-recruiting chemokines when stimulated by antibody-coated tumor cells, revealing that positive regulation of NK chemotaxis is embedded in a network of reciprocal immune cell recruitment. More recent studies have identified ion channels and immune checkpoint molecules as modulators of NK cell tumor infiltration, expanding the mechanistic repertoire of GO:2000503 [6,7]. For researchers, GO:2000503 provides a controlled vocabulary to annotate experiments that measure enhanced NK cell migration, whether driven by chemokines, cytokines, tumor microenvironment cues or genetic perturbations [2,5,6]. It also enables functional enrichment analysis of transcriptomic and proteomic datasets where NK cell recruitment signatures are interrogated in cancer, infection and inflammatory disease [1,3,8].
positive regulation of natural killer cell chemotaxis At A Glance
| GO ID | GO:2000503 |
|---|---|
| GO term | positive regulation of natural killer cell chemotaxis |
| Ontology | biological_process |
| Synonym | None listed in QuickGO |
| Major function | Increases the frequency, rate or extent of NK cell chemotaxis |
| Parent process | Regulation of natural killer cell chemotaxis |
| Related cell type | Natural killer (NK) cells |
| Key molecular drivers | Chemokines such as MCP-1, MCP-2, MCP-3; ion channels such as KCa3.1; immune receptors such as IL-1R8 |
| Disease relevance | Tumor immune evasion, lymphoma prognosis, inflammatory recruitment |
| Research methods | Chemotaxis assays, cytokine profiling, CRISPR screens, bioinformatic deconvolution |
What Is GO:2000503?
In plain terms, GO:2000503 covers any biological event that makes natural killer cells migrate more actively toward a chemical signal. The official QuickGO definition states: Any process that activates or increases the frequency, rate or extent of natural killer cell chemotaxis. This is a biological_process term that acts as a positive regulator of the parent process natural killer cell chemotaxis. It does not describe the chemotaxis itself but the upstream or concurrent signals, receptors, cytokines, chemokines and cellular changes that amplify it. A process is annotated to GO:2000503 when experimental evidence shows that perturbing it increases NK cell directional migration, for example by adding a chemokine, expressing a receptor, or knocking down an inhibitor [2,6,7].
Why Is positive regulation of natural killer cell chemotaxis Important in Cell Biology?
GO:2000503 matters because the ability of NK cells to reach a target tissue determines whether innate immunity can control tumors or infections at that site. Positive regulation of NK cell chemotaxis is therefore a checkpoint for immune surveillance: without it, NK cells remain in circulation or in lymphoid organs and cannot deliver cytotoxic hits [2,5]. Experimental evidence shows that chemokines directly induce NK cell migration, that NK cells reciprocally recruit T cells through chemokine production, and that ion channel activity and immune receptor expression tune NK cell tumor infiltration and patient prognosis [6,7]. Because these mechanisms are genetically and pharmacologically tractable, GO:2000503 is a productive entry point for cancer immunology, immunotherapy response prediction and immune cell engineering.
• Defines a measurable step in innate immune surveillance: NK cells must migrate to the tumor or infection site to kill.
• Chemokines MCP-1, MCP-2 and MCP-3 directly induce NK cell migration, providing druggable recruitment axes.
• NK cell-derived chemokines recruit T cells, linking GO:2000503 to adaptive immune amplification.
• KCa3.1 channel activity regulates tumor infiltration of functionally competent NK cells in head and neck cancer.
• IL-1R8 expression in diffuse large B-cell lymphoma regulates NK cell recruitment and influences patient prognosis.
• Immune deconvolution and Mendelian randomization studies use NK chemotaxis signatures to link molecular candidates to disease.
• Regulatory T cell differentiation and chemotaxis programs can drive immune evasion in pancreatic ductal adenocarcinoma, highlighting the balance of pro- and anti-recruitment signals.
• Collagen type VI alpha 6 chain has been proposed as a tumor suppressor with an immune regulation perspective, showing extracellular matrix genes can shape immune recruitment.
• CRISPR knockout and knock-in models allow causal testing of candidate regulators of NK chemotaxis [6,7].
• The term supports standardized annotation and enrichment analysis across cancer, infection and inflammation datasets [1,3,8].
What Happens During positive regulation of natural killer cell chemotaxis?
Chemokine sensing and receptor activation
In simple terms: NK cells sniff out chemical signals released by other cells and start moving toward them.
The initiating step of positive regulation of NK cell chemotaxis is the detection of chemotactic cues by NK cell surface receptors. Monocyte chemotactic protein-1 (MCP-1/CCL2), MCP-2 (CCL8) and MCP-3 (CCL7) were shown to induce NK cell migration in vitro, establishing chemokine sensing as a direct positive regulatory input. These signals convert an extracellular gradient into intracellular signaling that polarizes the NK cell and initiates directed motility. Because the process is defined as positive regulation, any factor that increases the sensitivity, number or signaling efficiency of these chemokine receptors on NK cells is annotated under GO:2000503.
Cytokine and tumor microenvironment amplification
In simple terms: Signals from tumors and immune cells can boost the chemotactic response, making NK cells move faster or in larger numbers.
Beyond direct chemokine sensing, the tumor microenvironment and cytokine milieu amplify NK cell recruitment. NK cells produce T cell-recruiting chemokines in response to antibody-coated tumor cells, demonstrating that activation by tumor-bound antibodies can positively regulate chemokine output and downstream immune cell recruitment. This amplification loop means that positive regulation of NK cell chemotaxis is not only about NK cells responding to gradients but also about NK cells shaping gradients that recruit additional effectors. In diffuse large B-cell lymphoma, IL-1R8 expression regulates NK cell recruitment, indicating that immune receptor signaling in the tumor can set the threshold for NK cell infiltration.
Ion channel and biophysical control of migration
In simple terms: Ion channels act like gates that help NK cells squeeze through tissues and keep moving.
Ion channels contribute to the biophysical capacity of NK cells to migrate and infiltrate tumors. KCa3.1 channels regulate the tumor infiltration of functionally competent NK cells in head and neck cancer, linking calcium-activated potassium conductance to NK cell motility and tissue penetration. This step represents a non-chemokine layer of positive regulation: even when chemokine gradients are present, ion channel activity may be required for NK cells to traverse tumor stroma and maintain function. Such mechanisms expand the set of experimental targets that can be annotated to GO:2000503 beyond classical chemokine-receptor pairs.
Extracellular matrix and tissue remodeling cues
In simple terms: The material around a tumor can either help or block NK cells from getting in.
Extracellular matrix composition influences immune cell recruitment and can therefore modulate positive regulation of NK cell chemotaxis. Collagen type VI alpha 6 chain has been studied as a potential tumor suppressor in breast cancer from an immune regulation perspective, suggesting that matrix genes can shape immune cell infiltration. Although the precise molecular link to NK cell chemotaxis requires further experimental validation, matrix remodeling is a recognized variable in immune recruitment assays and should be controlled when studying GO:2000503. This subsection emphasizes that positive regulation can arise from tissue-level changes, not only from soluble chemokines.
Integration with systemic immune programs
In simple terms: NK cell recruitment is part of a bigger immune plan that can be turned up or down by other immune cells.
Positive regulation of NK cell chemotaxis is embedded in broader immune programs. Regulatory T cell differentiation and chemotaxis can drive immune evasion in pancreatic ductal adenocarcinoma, illustrating that opposing immune cell programs can indirectly suppress or redirect NK cell recruitment. Bioinformatics and Mendelian randomization analyses of immune-related disease datasets can identify systemic signatures that correlate with NK chemotaxis pathways. Therefore, GO:2000503 should be interpreted within the context of the whole immune microenvironment rather than as an isolated NK cell behavior [1,3].
Key Genes Involved in GO:2000503 positive regulation of natural killer cell chemotaxis
The following genes and proteins have been experimentally or analytically linked to positive regulation of natural killer cell chemotaxis or to NK cell recruitment in disease contexts.
| Gene | Major Role | Research Relevance |
|---|---|---|
| CCL2 (MCP-1) | Induces NK cell migration | Foundational chemokine for NK chemotaxis assays |
| CCL8 (MCP-2) | Induces NK cell migration | Chemokine gradient control in vitro |
| CCL7 (MCP-3) | Induces NK cell migration | Chemokine-driven NK recruitment |
| KCNN4 (KCa3.1) | Regulates NK cell tumor infiltration | Ion channel target in head and neck cancer |
| IL1R8 | Regulates NK cell recruitment in lymphoma | Prognostic immune receptor in DLBCL |
| GNLY (Granulysin) | Cytotoxic and immune effector molecule | Biology and clinical relevance in immunity |
| COL6A6 | Extracellular matrix tumor suppressor candidate | Immune regulation perspective in breast cancer |
| LMO7 | Regulatory T cell differentiation and chemotaxis | Immune evasion in pancreatic ductal adenocarcinoma |
| FOXP3 | Regulatory T cell lineage | Indirect modulation of immune recruitment |
| CCR2 | Chemokine receptor for MCP family | Candidate receptor for NK chemotaxis |
| CCR5 | Chemokine receptor for MCP family | Candidate receptor for NK chemotaxis |
| IFNG | NK cell effector cytokine | Functional competence of infiltrating NK cells |
| PRF1 | Cytotoxic granule protein | NK cell cytotoxic function after recruitment |
| GZMB | Cytotoxic granule protein | NK cell effector function |
| KLRD1 (CD94) | NK cell receptor | NK cell recognition and activation |
| FCGR3A (CD16) | Antibody-dependent activation receptor | Antibody-coated tumor cell response |
| CXCL10 | T cell-recruiting chemokine | NK cell-derived chemokine output |
How Is positive regulation of natural killer cell chemotaxis Regulated?
Positive regulation of NK cell chemotaxis is controlled at multiple levels. Chemokine availability and receptor expression set the primary threshold, as MCP-1, MCP-2 and MCP-3 directly induce NK cell migration. Cytokine and antibody-mediated activation can increase NK cell chemokine production, creating positive feedback that recruits additional immune cells. Ion channel activity, exemplified by KCa3.1, regulates the ability of functionally competent NK cells to infiltrate tumors, indicating that biophysical properties of the NK cell membrane are part of the regulatory logic. Immune receptor expression in the tumor microenvironment, such as IL-1R8 in diffuse large B-cell lymphoma, can regulate NK cell recruitment and influence patient prognosis. Finally, opposing immune programs such as regulatory T cell differentiation and chemotaxis can indirectly shape the net recruitment of NK cells in pancreatic ductal adenocarcinoma. Together these layers determine whether GO:2000503 is active in a given tissue context.
positive regulation of natural killer cell chemotaxis and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| KCNN4 | Head and neck cancer NK cell infiltration | KCNN4 knockout NK cell line with chemotaxis assay |
| IL1R8 | Diffuse large B-cell lymphoma prognosis | IL1R8 overexpression in lymphoma cell line co-cultured with NK cells |
| LMO7 | Pancreatic ductal adenocarcinoma immune evasion | LMO7 knockout in pancreatic cancer models with immune profiling |
| COL6A6 | Breast cancer tumor suppression and immune regulation | COL6A6 knock-in breast cancer cell line with immune deconvolution |
| CCL2/CCL7/CCL8 | Chemokine-driven NK recruitment | Chemokine knockout or overexpression with transwell migration assays |
Cancer immune surveillance and evasion
NK cell infiltration into tumors is a determinant of immune control, and positive regulation of NK cell chemotaxis is required for NK cells to reach malignant tissue [2,5]. In head and neck cancer, KCa3.1 channels regulate the tumor infiltration of functionally competent NK cells, linking this GO term to a specific solid tumor context. In diffuse large B-cell lymphoma, IL-1R8 expression regulates NK cell recruitment and influences patient prognosis, showing that the same process can be prognostic in hematologic malignancy. Pancreatic ductal adenocarcinoma provides an example of immune evasion through regulatory T cell differentiation and chemotaxis, which can shift the balance away from effective NK cell recruitment. These studies collectively position GO:2000503 as a process whose enhancement or suppression has direct tumor immunology consequences.
Inflammatory and metabolic disease connections
Because chemokine gradients are shared across inflammatory conditions, positive regulation of NK cell chemotaxis can be relevant beyond oncology. Bioinformatics and Mendelian randomization analyses have been used to link immune and metabolic disease traits, including non-alcoholic fatty liver disease and heart failure, to immune cell signatures. Such analyses can generate hypotheses about whether NK cell recruitment pathways contribute to tissue inflammation in metabolic disease. Experimental validation in appropriate models is required before causal claims are made, but the computational framework illustrates how GO:2000503 can be interrogated in complex disease datasets.
Extracellular matrix and tumor suppressor biology
Extracellular matrix genes can influence immune cell recruitment and tumor behavior. Collagen type VI alpha 6 chain has been evaluated as a potential tumor suppressor in breast cancer from an immune regulation perspective, suggesting that matrix composition may affect immune cell infiltration. While direct evidence for NK cell chemotaxis regulation by COL6A6 remains to be established, this line of research highlights the importance of considering matrix-immune interactions when studying GO:2000503. Experimental models that manipulate matrix genes alongside NK cell migration assays can test whether matrix remodeling positively regulates NK cell recruitment.
From positive regulation of natural killer cell chemotaxis-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Does a candidate gene increase NK cell migration? | CRISPR knockout of the gene in NK cells followed by transwell chemotaxis assay [2,6] |
| Does a point mutation in a chemokine receptor alter NK recruitment? | Point-mutation knock-in of the receptor in NK cell line with chemokine gradient |
| Does overexpression of a tumor-derived factor enhance NK infiltration? | Overexpression cell model co-cultured with primary NK cells |
| Does a tagged protein localize during NK cell migration? | Tagged knock-in of the gene in NK cells with live imaging |
| Which genes regulate NK cell tumor infiltration? | Genome-wide CRISPR library screening in NK cells with tumor infiltration readout |
| Can bioinformatic signatures predict NK chemotaxis activity? | Immune deconvolution of transcriptomic datasets from patient cohorts [1,8] |
How to Study the positive regulation of natural killer cell chemotaxis Process
| Method | What It Measures | Typical Application |
|---|---|---|
| Transwell chemotaxis assay | Number of NK cells migrating toward a chemokine | Testing MCP-1/2/3-induced NK migration |
| Microfluidic gradient assay | Directionality and speed of NK cell movement | Quantifying positive regulation of chemotaxis |
| Multiplex cytokine profiling | Secreted chemokine levels | NK cell response to antibody-coated tumor cells |
| RNA sequencing | Transcriptional changes in chemokine and receptor genes | Identifying regulators of NK recruitment [5,6] |
| CRISPR knockout screen | Genes required for NK cell tumor infiltration | Discovering positive regulators such as KCa3.1 |
| CRISPR activation screen | Genes whose overexpression enhances migration | Finding gain-of-function chemotaxis drivers |
| Immune deconvolution | Estimated NK cell infiltration from bulk transcriptomes | Linking GO:2000503 signatures to disease [1,8] |
| Live imaging | Real-time NK cell motility in 3D matrices | Visualizing ion channel and matrix effects [6,8] |
Chemotaxis and migration assays
Transwell and microfluidic chemotaxis assays are the primary methods to measure positive regulation of NK cell chemotaxis. In these assays, NK cells are placed in a gradient of chemokines such as MCP-1, MCP-2 or MCP-3, and the number of migrated cells is quantified. Positive regulation is demonstrated when a perturbation increases migration relative to control. These assays can be combined with cytokine stimulation or antibody-coated tumor cells to mimic the tumor microenvironment.
Cytokine and chemokine profiling
Because NK cells produce T cell-recruiting chemokines in response to antibody-coated tumor cells, profiling secreted chemokines is a direct way to assess positive regulation of recruitment programs. Multiplex immunoassays or RNA sequencing of chemokine genes can quantify changes in CCL2, CCL7, CCL8, CXCL10 and related factors [2,5]. Such profiling links molecular perturbations to the chemotactic output that defines GO:2000503.
CRISPR screening and functional genomics
Genome-wide CRISPR knockout or activation screens in NK cells can identify genes whose loss or gain changes tumor infiltration or chemotaxis. KCa3.1 was identified as a regulator of NK cell tumor infiltration using functional approaches, illustrating how ion channel genes can emerge from such screens. CRISPR screening combined with chemotaxis readouts provides an unbiased route to discover new positive regulators annotated to GO:2000503.
Bioinformatic immune deconvolution
Transcriptomic datasets from patient cohorts can be deconvoluted to estimate NK cell infiltration and chemotaxis signatures. Bioinformatics and Mendelian randomization analyses have been used to connect immune signatures to disease traits such as non-alcoholic fatty liver disease and heart failure. Similar approaches can test whether GO:2000503-related gene sets are enriched in disease states and generate hypotheses for experimental validation [1,8].
How CRISPR Can Be Used to Study GO:2000503 positive regulation of natural killer cell chemotaxis
Knockout
CRISPR knockout of candidate genes in NK cell lines or primary NK cells is used to test whether a gene is required for positive regulation of NK cell chemotaxis. For example, knocking out KCNN4 (KCa3.1) can reduce NK cell tumor infiltration, directly linking the channel to GO:2000503. Knockout of chemokine genes such as CCL2, CCL7 or CCL8 can abolish gradient formation and reduce NK cell migration in co-culture systems. Knockout models provide loss-of-function evidence that a gene positively regulates the process.
Point Mutation
Point-mutation knock-in can dissect specific residues in chemokine receptors or ion channels that are required for enhanced NK cell migration. For example, mutating a phosphorylation site in a chemokine receptor or a pore residue in KCa3.1 can separate signaling from conductance functions [2,6]. These models are valuable when a gene has multiple domains and the researcher needs to attribute the chemotaxis phenotype to a specific molecular activity. Point mutations also help validate drug binding sites identified in silico.
Knock-in
Knock-in of tagged or reporter versions of genes such as KCNN4 or IL1R8 allows visualization and quantification of protein localization during NK cell migration [6,7]. Knock-in of a fluorescent tag can reveal whether the protein traffics to the leading edge of a migrating NK cell. Knock-in of disease-associated variants can test whether a patient-derived mutation alters NK cell recruitment in a controlled genetic background. These models bridge GO:2000503 annotation with clinical variant interpretation.
Overexpression
Overexpression of candidate genes in NK cells or tumor cells can test gain-of-function effects on NK cell chemotaxis. Overexpressing IL-1R8 in lymphoma cells has been used to study NK cell recruitment and prognosis, showing that tumor-side overexpression can regulate the process. Overexpression of chemokines such as CCL2 or CCL7 in tumor models can increase NK cell infiltration and is a direct test of positive regulation. Overexpression models are particularly useful when the endogenous expression level is low or when a gain-of-function hypothesis is being tested.
How EDITGENE Supports positive regulation of natural killer cell chemotaxis Research
Researchers studying positive regulation of natural killer cell chemotaxis-related genes often need to determine whether a candidate gene is causally involved in NK cell recruitment or merely correlated with it. Establishing causality requires controlled genetic perturbation in relevant cell models, followed by functional chemotaxis or infiltration assays. EDITGENE provides the CRISPR tools and cell model engineering services needed to move from bioinformatic hypothesis to experimental validation for GO:2000503 research.
Contact EDITGENE today to design your custom CRISPR model for positive regulation of natural killer cell chemotaxis research.
Frequently Asked Questions About positive regulation of natural killer cell chemotaxis
What is GO:2000503 positive regulation of natural killer cell chemotaxis?
GO:2000503 is a Gene Ontology biological process term defined as any process that activates or increases the frequency, rate or extent of natural killer cell chemotaxis, the directed migration of NK cells along chemical gradients.
What genes are involved in positive regulation of natural killer cell chemotaxis?
Genes and proteins experimentally linked to this process include chemokines CCL2 (MCP-1), CCL8 (MCP-2) and CCL7 (MCP-3), the ion channel KCNN4 (KCa3.1), the immune receptor IL1R8, and matrix gene COL6A6 [2,6,7,8].
How do chemokines positively regulate NK cell chemotaxis?
Monocyte chemotactic protein-1, -2 and -3 directly induce NK cell migration, providing the chemotactic gradient that activates directed movement.
What role do NK cells play in recruiting other immune cells?
NK cells produce T cell-recruiting chemokines in response to antibody-coated tumor cells, creating a positive feedback loop that amplifies immune cell recruitment.
Which ion channels regulate NK cell tumor infiltration?
KCa3.1 channels regulate the tumor infiltration of functionally competent NK cells in head and neck cancer, linking ion conductance to NK cell motility.
How is IL-1R8 related to NK cell recruitment?
IL-1R8 expression in diffuse large B-cell lymphoma regulates NK cell recruitment and influences patient prognosis.
What diseases are associated with defective NK cell chemotaxis?
Cancer immune evasion is the best studied context, including head and neck cancer, diffuse large B-cell lymphoma and pancreatic ductal adenocarcinoma, where NK cell recruitment affects tumor control and prognosis [3,6,7].
What methods are used to study positive regulation of NK cell chemotaxis?
Common methods include transwell and microfluidic chemotaxis assays, cytokine profiling, CRISPR knockout or activation screens, live imaging and bioinformatic immune deconvolution [1,2,5,6].
Can CRISPR screens identify new regulators of NK cell chemotaxis?
Yes, genome-wide CRISPR screens in NK cells with tumor infiltration or migration readouts can discover genes such as KCa3.1 that regulate NK cell recruitment.
How can I model GO:2000503 in the lab with CRISPR?
You can use CRISPR knockout to test loss-of-function, point-mutation knock-in to dissect residues, tagged knock-in for imaging, or overexpression to test gain-of-function in NK cell chemotaxis assays [2,6,7].
Conclusion
GO:2000503 positive regulation of natural killer cell chemotaxis captures a critical control point in innate immunity: the signals and cellular properties that increase NK cell migration toward tumors, infections and inflamed tissues [2,5]. Experimental evidence from chemokine biology, ion channel physiology and immune receptor studies shows that this process is genetically and pharmacologically tractable, with direct implications for cancer prognosis and immunotherapy [6,7]. As immune deconvolution and CRISPR screening technologies mature, the list of positive regulators annotated to GO:2000503 will continue to grow, offering new targets for therapeutic enhancement of NK cell recruitment [1,3,8].
References
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- 3. Dai S et al.. 2025. LIM domain only 7: a novel driver of immune evasion through regulatory T cell differentiation and chemotaxis in pancreatic ductal adenocarcinoma.. Cell Death Differ 32(2):271-290 PMID: 39143228
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- 5. Roda JM et al.. 2006. Natural killer cells produce T cell-recruiting chemokines in response to antibody-coated tumor cells.. Cancer Res 66(1):517-26 PMID: 16397268
- 6. Alshwimi AO et al.. 2025. KCa3.1 channels regulate the tumor infiltration of functionally competent NK cells in head and neck cancer.. Sci Rep 15(1):36360 PMID: 41107295
- 7. Yu M et al.. 2023. IL-1R8 expression in DLBCL regulates NK cell recruitment and influences patient prognosis.. Funct Integr Genomics 23(4):328 PMID: 37907630
- 8. Li JD et al.. 2025. The role of collagen type VI alpha 6 chain as a potential tumor suppressor in breast cancer: an immune regulation perspective.. BMC Cancer 25(1):1363 PMID: 40846911
