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 (657 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
Specialized cells of the hematopoietic system that have branch-like extensions. They are found throughout the lymphatic system, and in non-lymphoid tissues such as SKIN and the epithelia of the intestinal, respiratory, and reproductive tracts. They trap and process antigens, and present them to t-cells, thereby stimulating cell-mediated immunity. They are different from the non-hematopoietic follicular dendritic cells, which have a similar morphology and immune system function, but with respect to humoral immunity (antibody production).
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: Cell, Dendritic; Cells, Dendritic; Dendritic Cell; Veiled Cells; Cells, Veiled; Cell, Veiled; Veiled Cell; Interdigitating Cells.
Where it fits in the MeSH classification
- Broader topics
- Antigen-Presenting Cells; Epithelial Cells; Mononuclear Phagocyte System
- Narrower topics
- Langerhans Cells
Related concepts
- Antigens
- T-Lymphocytes
- Cell-Mediated Immunity
- Follicular Dendritic Cells
- Antibody Production
Research landscape
PubMed indexes 58,968 records tagged with the MeSH heading “Dendritic Cells” (counts retrieved 2026-10-31). 9,898 of them (16.8%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 22,596 records.
Reviews account for 8,907 records (15.1%) and meta-analyses for 62. Randomized controlled trials number 288 (0.5%) 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 | 6,702 |
| 2000-2009 | 19,772 |
| 2010-2019 | 22,596 |
| 2020 onward | 9,898 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 8,907 | 15.1% |
| Meta-analyses | 62 | 0.1% |
| Randomized controlled trials | 288 | 0.5% |
Method: PubMed query "Dendritic Cells"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in anatomy and physiology
Anatomy describes how body structures are built and physiology describes how they normally work, so most findings here are descriptive or mechanistic rather than evidence about treatment. Much of what is known comes from dissection, imaging, tissue studies and experiments in animals, and measurements in healthy volunteers can differ from those in people with disease or at different ages. Normal ranges vary between individuals and populations. Check whether a result was measured in people or in another species, the age and health of the participants, and the method used.
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.
TNF and type I interferon crosstalk controls the fate and function of plasmacytoid dendritic cells [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Plasmacytoid dendritic cells (pDCs) are major producers of type I interferon (IFN-I), an important antiviral cytokine, and activity of these cells must be tightly controlled to prevent harmful inflammation and autoimmunity.
- Closing excerpt
- This work identifies the pDC-to-cDC reprogramming trajectory and unveils a mechanistic framework for harnessing it therapeutically.
- 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 (153 words)
Plasmacytoid dendritic cells (pDCs) are major producers of type I interferon (IFN-I), an important antiviral cytokine, and activity of these cells must be tightly controlled to prevent harmful inflammation and autoimmunity. Evidence exists that one regulatory mechanism is a fate-switching process from an IFN-I-secreting pDC to a professional antigen-presenting conventional dendritic cell (cDC) that lacks IFN-I-secreting capacity. However, this differentiation process is controversial owing to limitations in tracking the fate of individual cells over time. Here we use single-cell omics and functional experiments to show that activated human pDCs can lose their identity as IFN-I-secreting cells and acquire the transcriptional, epigenetic and functional features of cDCs. This pDC fate-switching process is promoted by tumor necrosis factor but blocked by IFN-I. Importantly, it occurs in vivo during human skin inflammatory diseases and injury, and physiologically in elderly people. This work identifies the pDC-to-cDC reprogramming trajectory and unveils a mechanistic framework for harnessing it therapeutically.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40796660 · DOI · PMC12396960
Mature and migratory dendritic cells promote immune infiltration and response to anti-PD-1 checkpoint blockade in metastatic melanoma [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Immune checkpoint inhibitors (ICIs) have revolutionized cancer therapy, yet most patients fail to achieve durable responses.
- Closing excerpt
- Further characterization of mregDCs versus conventional dendritic cells (cDC1/cDC2) highlights their unique transcriptional, epigenetic (single-nucleus ATAC-seq data for cDCs from 14 matched samples), and interaction profiles, offering new insights for improving immunotherapy response and guiding future combination treatments.
- 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 (156 words)
Immune checkpoint inhibitors (ICIs) have revolutionized cancer therapy, yet most patients fail to achieve durable responses. To better understand the tumor microenvironment (TME), we analyze single-cell RNA-seq (~189 K cells) from 36 metastatic melanoma samples, defining 14 cell types, 55 subtypes, and 15 transcriptional hallmarks of malignant cells. Correlations between cell subtype proportions reveal six distinct clusters, with a mature dendritic cell subtype enriched in immunoregulatory molecules (mregDC) linked to naive T and B cells. Importantly, mregDC abundance predicts progression-free survival (PFS) with ICIs and other therapies, especially when combined with the TCF7 + /- CD8 T cell ratio. Analysis of an independent cohort (n = 318) validates mregDC as a predictive biomarker for anti-CTLA-4 plus anti-PD-1 therapies. Further characterization of mregDCs versus conventional dendritic cells (cDC1/cDC2) highlights their unique transcriptional, epigenetic (single-nucleus ATAC-seq data for cDCs from 14 matched samples), and interaction profiles, offering new insights for improving immunotherapy response and guiding future combination treatments.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40890106 · DOI · PMC12402436
The tumor-sentinel lymph node immuno-migratome reveals CCR7⁺ dendritic cells drive response to sequenced immunoradiotherapy [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Surgical ablation or broad radiation of tumor-draining lymph nodes can eliminate the primary tumor response to immunotherapy, highlighting the crucial role of these nodes in mediating the primary tumor response.
- Closing excerpt
- Overall, this work supports rationally sequencing immune-sensitizing, lymphatic-preserving, tumor-directed radiotherapy followed by immune checkpoint inhibition to optimize tumor response to immunoradiotherapy by driving activated dendritic cells to draining sentinel lymph nodes.
- 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 (188 words)
Surgical ablation or broad radiation of tumor-draining lymph nodes can eliminate the primary tumor response to immunotherapy, highlighting the crucial role of these nodes in mediating the primary tumor response. Here, we show that immunoradiotherapy efficacy is dependent on treatment sequence and migration of modulated dendritic cells from tumor to sentinel lymph nodes. Using a tamoxifen-inducible reporter paired with CITE-sequencing in a murine model of oral cancer, we comprehensively characterize tumor immune cellular migration through lymphatic channels to sentinel lymph nodes at single-cell resolution, revealing a unique immunologic niche defined by distinct cellular phenotypic and transcriptional profiles. Through a structured approach of sequential immunomodulatory radiotherapy and checkpoint inhibition, we show that sequenced, lymphatic-sparing, tumor-directed radiotherapy followed by PD-1 inhibition achieves complete and durable tumor responses. Mechanistically, this treatment approach enhances migration of activated CCR7+ dendritic cell surveillance across the tumor-sentinel lymph node axis, revealing a shift from their canonical role in promoting tolerance to driving antitumor immunity. Overall, this work supports rationally sequencing immune-sensitizing, lymphatic-preserving, tumor-directed radiotherapy followed by immune checkpoint inhibition to optimize tumor response to immunoradiotherapy by driving activated dendritic cells to draining sentinel lymph nodes.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40675962 · DOI · PMC12271439
Positioning and reversible suppression of CCR7+ dendritic cells in perivascular tumor niches shape cancer immunity [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Tumor-resident CCR7+ dendritic cells (DCs) are key determinants of antitumor T cell responses.
- Closing excerpt
- Modulating the mechanisms that form and restrain CCR7+ DC perivascular immune hubs may improve cancer immunotherapy.
- 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 (160 words)
Tumor-resident CCR7+ dendritic cells (DCs) are key determinants of antitumor T cell responses. Here, we examined the localization of CCR7+ DCs within tumors and the impact of this positioning on antitumor immunity. Spatial, single-cell, and intravital analyses of human cancers and mouse models reveal that CCR7+ DCs form perivascular clusters. Fibroblasts surrounding venous blood vessels produced CCL19, guiding CCR7+ DCs into perivascular niches. Regulatory T (Treg) cells frequently contact perivascular CCR7+ DCs, suppressing CD40 expression and CD4+ and CD8+ T cell activation. Treg cell depletion restored CD40 expression by CCR7+ DCs, enhanced immunostimulatory programs, and improved T cell-dependent tumor control. Anti-PD-1 not only increased perivascular CCR7+ DC clustering and IL-12 production but also strengthened Treg-DC interactions through a CCL22-dependent mechanism, limiting therapeutic efficacy. CCR7+ DCs expressed both co-stimulatory and co-inhibitory molecules, which may underlie their capacity for antitumor activation and concurrent vulnerability to suppression. Modulating the mechanisms that form and restrain CCR7+ DC perivascular immune hubs may improve cancer immunotherapy.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41421339 · DOI · PMC12882814
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 Dendritic cell subsets in cancer immunity and tumor antigen sensing [5]
- Research article Dendritic cell migration in inflammation and immunity [6]
- Research article Dendritic cell biology and its role in tumor immunotherapy [7]
- Research article Antigen presentation by dendritic cells and their instruction of CD4+ T helper cell responses [8]
- Research article Dendritic cells as shepherds of T cell immunity in cancer [9]
- Research article Genetic models of human and mouse dendritic cell development and function [10]
References
- Arroyo Hornero R, Maqueda-Alfaro RA, Solís-Barbosa MA, Leylek RA, Medina Chavez O, Martinez OM, et al.. TNF and type I interferon crosstalk controls the fate and function of plasmacytoid dendritic cells. . 2025. PMID 40796660 · DOI · PMC12396960
- Yang J, Wang C, Fu D, Ho LL, Galani K, Chen L, et al.. Mature and migratory dendritic cells promote immune infiltration and response to anti-PD-1 checkpoint blockade in metastatic melanoma. . 2025. PMID 40890106 · DOI · PMC12402436
- Saddawi-Konefka R, Msari RA, Tang S, Philips C, Sadat S, Clubb LM, et al.. The tumor-sentinel lymph node immuno-migratome reveals CCR7⁺ dendritic cells drive response to sequenced immunoradiotherapy. . 2025. PMID 40675962 · DOI · PMC12271439
- Zitti B, Duval F, Wirapati P, Hicham M, Xie Y, Oh J, et al.. Positioning and reversible suppression of CCR7+ dendritic cells in perivascular tumor niches shape cancer immunity. . 2026. PMID 41421339 · DOI · PMC12882814
- Del Prete A, Salvi V, Soriani A, Laffranchi M, Sozio F, Bosisio D, et al.. Dendritic cell subsets in cancer immunity and tumor antigen sensing. Cell Mol Immunol. 2023. PMID 36949244 · DOI · PMC10203372
- Liu J, Zhang X, Cheng Y, Cao X. Dendritic cell migration in inflammation and immunity. Cell Mol Immunol. 2021. PMID 34302064 · DOI · PMC8298985
- Wang Y, Xiang Y, Xin VW, Wang XW, Peng XC, Liu XQ, et al.. Dendritic cell biology and its role in tumor immunotherapy. J Hematol Oncol. 2020. PMID 32746880 · DOI · PMC7397618
- Hilligan KL, Ronchese F. Antigen presentation by dendritic cells and their instruction of CD4+ T helper cell responses. Cell Mol Immunol. 2020. PMID 32433540 · DOI · PMC7264306
- Pittet MJ, Di Pilato M, Garris C, Mempel TR. Dendritic cells as shepherds of T cell immunity in cancer. Immunity. 2023. PMID 37708889 · DOI · PMC10591862
- Anderson DA, Dutertre CA, Ginhoux F, Murphy KM. Genetic models of human and mouse dendritic cell development and function. Nat Rev Immunol. 2021. PMID 32908299 · DOI · PMC10955724
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.