---
title: "Plasma small extracellular vesicles in head and neck cancer drive dysfunctional T-cell phenotypes"
id: "british-journal-of-cancer-0-small-extracellular-vesicles-from-the-plasma-of-head-and-neck-cancer-patients"
canonical_url: "https://medichelpline.com/clinical-feed/british-journal-of-cancer-0-small-extracellular-vesicles-from-the-plasma-of-head-and-neck-cancer-patients"
content_type: "clinical_feed_article"
specialty: "Oncology"
source_name: "British Journal of Cancer"
source_url: "https://www.nature.com/articles/s41416-026-03606-8"
published_at: "2026-09-26T12:00:00.000Z"
evidence_level: "Journal Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Plasma small extracellular vesicles in head and neck cancer drive dysfunctional T-cell phenotypes
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/british-journal-of-cancer-0-small-extracellular-vesicles-from-the-plasma-of-head-and-neck-cancer-patients
- **Specialty:** [Oncology](https://medichelpline.com/clinical-feed/oncology.md)
- **Primary Source:** British Journal of Cancer
- **Source URL:** [Original Journal Publication](https://www.nature.com/articles/s41416-026-03606-8)
- **Published At:** 2026-09-26T12:00:00.000Z
- **Evidence Rating:** Journal Feed
## Executive GIST (TL;DR)
- Head and neck cancer (HNC) is immunosuppressive; **small extracellular vesicles (sEVs)** released into plasma are candidate mediators of systemic immune dysfunction. - The study isolated plasma sEVs by size-exclusion chromatography (SEC) from HNC patients (N = 50), recovered/no evident disease patients (NED, N = 20) and healthy donors (HD, N = 22); samples were collected 2019–2023. - Isolation workflow included sequential centrifugation (2000 × g then 14,000 × g), 0.22 µm filtration, self-made Sepharose CL-2B SEC columns and collection of the fourth 1 mL PBS eluate fraction. - Patient-derived plasma sEVs inhibited both **CD4+** and **CD8+ T-cell** function in vitro and promoted **CD8+ T-cell apoptosis**; these effects correlated with disease progression. - Plasma sEVs increased conversion of ATP to AMP and altered expression of ectonucleotidases, implicating the **adenosinergic pathway** and enzymes **CD39** and **CD73** in sEV-mediated immunosuppression. - Immune-checkpoint (IC) profiling showed differential effects: CD4+ T cells exposed to HNC sEVs had higher **TIGIT** and **CTLA-4** but lower **BTLA**, **PD‑1**, and **LAG‑3**; CD8+ T cells showed a broad downregulation of both inhibitory and stimulatory ICs. - Blockade of PD‑1 (PD‑1 inhibition) did not fully abrogate the suppressive effects of plasma sEVs on T cells, indicating that sEV-mediated suppression is only partially dependent on the PD‑1/PD‑L1 axis. - The authors conclude plasma sEVs contribute to systemic immune modulation in HNC and may affect responses to immunotherapy; they recommend further investigation into sEV effects and potential biomarker or therapeutic relevance. - Specific experimental details beyond the Methods subsection (for example full TEM results, complete characterisation data, quantitative effect sizes, statistical analyses, and extended results) were not reported in the provided source excerpt.
## Clinical Analysis & Structured Key Points
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[nature](https://www.nature.com/) 2. [british journal of cancer](https://www.nature.com/bjc) 3. [articles](https://www.nature.com/bjc/articles?type=article) 4. article Small extracellular vesicles from the plasma of head and neck cancer patients induce dysfunctional T cell phenotypes [ Download PDF ](https://www.nature.com/articles/s41416-026-03606-8.pdf) [ Download PDF ](https://www.nature.com/articles/s41416-026-03606-8.pdf) * Article * [Open access](https://www.springernature.com/gp/open-science/about/the-fundamentals-of-open-access-and-open-research) * Published: 26 September 2026 Cellular and Molecular Biology # Small extracellular vesicles from the plasma of head and neck cancer patients induce dysfunctional T cell phenotypes * [Luisa Tengler](https://www.nature.com/articles/s41416-026-03606-8#auth-Luisa-Tengler-Aff1) [ORCID: orcid.org/0000-0003-3388-698X](https://orcid.org/0000-0003-3388-698X)[1](https://www.nature.com/articles/s41416-026-03606-8#Aff1), * [Edwin K. Jackson](https://www.nature.com/articles/s41416-026-03606-8#auth-Edwin_K_-Jackson-Aff2)[2](https://www.nature.com/articles/s41416-026-03606-8#Aff2), * [Karen Bieback](https://www.nature.com/articles/s41416-026-03606-8#auth-Karen-Bieback-Aff3)[3](https://www.nature.com/articles/s41416-026-03606-8#Aff3), * [Ralph Röth](https://www.nature.com/articles/s41416-026-03606-8#auth-Ralph-R_th-Aff4)[4](https://www.nature.com/articles/s41416-026-03606-8#Aff4), * [Stefanie Mellein](https://www.nature.com/articles/s41416-026-03606-8#auth-Stefanie-Mellein-Aff4)[4](https://www.nature.com/articles/s41416-026-03606-8#Aff4), * [Johann Kern](https://www.nature.com/articles/s41416-026-03606-8#auth-Johann-Kern-Aff1)[1](https://www.nature.com/articles/s41416-026-03606-8#Aff1), * [Marie-Nicole Theodoraki](https://www.nature.com/articles/s41416-026-03606-8#auth-Marie_Nicole-Theodoraki-Aff5) [ORCID: orcid.org/0000-0002-5491-1593](https://orcid.org/0000-0002-5491-1593)[5](https://www.nature.com/articles/s41416-026-03606-8#Aff5), * [Julia Schütz](https://www.nature.com/articles/s41416-026-03606-8#auth-Julia-Sch_tz-Aff1)[1](https://www.nature.com/articles/s41416-026-03606-8#Aff1), * [Lena Huber](https://www.nature.com/articles/s41416-026-03606-8#auth-Lena-Huber-Aff1)[1](https://www.nature.com/articles/s41416-026-03606-8#Aff1), * [Claudia Scherl](https://www.nature.com/articles/s41416-026-03606-8#auth-Claudia-Scherl-Aff1)[1](https://www.nature.com/articles/s41416-026-03606-8#Aff1), * [Nicole Rotter](https://www.nature.com/articles/s41416-026-03606-8#auth-Nicole-Rotter-Aff1)[1](https://www.nature.com/articles/s41416-026-03606-8#Aff1), * [Annette Affolter](https://www.nature.com/articles/s41416-026-03606-8#auth-Annette-Affolter-Aff1)[1](https://www.nature.com/articles/s41416-026-03606-8#Aff1) [na1](https://www.nature.com/articles/s41416-026-03606-8#na1) & * … * [Sonja Ludwig](https://www.nature.com/articles/s41416-026-03606-8#auth-Sonja-Ludwig-Aff1)[1](https://www.nature.com/articles/s41416-026-03606-8#Aff1) [na1](https://www.nature.com/articles/s41416-026-03606-8#na1) Show authors [_British Journal of Cancer_](https://www.nature.com/bjc) (2026) [Cite this article](https://www.nature.com/articles/s41416-026-03606-8#citeas) [ Save article ](https://www.nature.com/articles/s41416-026-03606-8/save-research?_csrf=iwaSmwM8TR9tXiXSnIHb50LK58heFqHk) [ View saved research ](https://www.nature.com/saved-research) ## Abstract ### Background Head and neck cancer (HNC) is highly immunosuppressive. Despite advances with immune checkpoint (IC) inhibitors, many HNC patients fail to respond. Tumour-derived small extracellular vesicles (sEVs) may contribute to immune evasion and therapy resistance, possibly by altering T-cell phenotypes. ### Method Plasma sEVs were isolated from HNC patient samples and controls via size-exclusion chromatography. The plasma sEVs were characterised and analysed for their effects on CD4⁺ and CD8⁺ T-cell function, IC levels and gene expression. ### Results HNC patient-derived sEVs inhibit CD4+ and CD8+ T-cell function and promote CD8+ T-cell apoptosis, correlating with disease progression. Plasma sEVs can enhance the conversion of ATP to AMP and modulate the expression of ectonucleotidases. IC profiling revealed complex alterations, with CD4⁺ T cells showing increased TIGIT and CTLA-4 but decreased BTLA, PD-1, and LAG-3 expression, whereas CD8⁺ T cells showed a downregulation of both inhibitory and stimulatory ICs. PD-1 blockade did not completely prevent sEV-mediated T-cell suppression. ### Conclusions Our findings suggest that plasma sEVs contribute to systemic immune modulation in HNC by inducing dysfunctional T-cell phenotypes. The ability of plasma-derived sEVs to modulate IC expression on T cells underscores the need for further investigation into their relevance for immunotherapeutic strategies in HNC. ### Explore related subjects Discover the latest articles and news in related subjects. * [Head and neck cancer](https://www.nature.com/subjects/head-and-neck-cancer) * [Immune evasion](https://www.nature.com/subjects/immune-evasion) * [Tumour biomarkers](https://www.nature.com/subjects/tumour-biomarkers) * [Tumour immunology](https://www.nature.com/subjects/tumour-immunology) ## Background Head and neck cancers (HNC) are among the top ten most common cancer types worldwide [[1](https://www.nature.com/articles/s41416-026-03606-8#ref-CR1 "Sung H, Ferlay J, Siegel RL, Laversanne M, Soerjomataram I, Jemal A, et al. Global cancer statistics 2020: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries. CA Cancer J Clin. 2021;71:209–49.")]. HNCs are often diagnosed at advanced stages, leading to poor therapeutic response and prognosis for many patients. One major feature of HNC is its highly immunosuppressive tumour microenvironment, characterised by the expression of inhibitory immune checkpoint molecules such as PD-1/PD-L1 and CTLA­4, which dampen antitumour T-cell responses [[2](https://www.nature.com/articles/s41416-026-03606-8#ref-CR2 "Whiteside TL. Head and neck carcinoma immunotherapy: facts and hopes. Clin Cancer Res. 2018;24:6–13.")]. Although immune checkpoint inhibitors (ICI), targeting PD-1 and CTLA-4, have improved outcomes for some patients, many fail to respond, indicating the involvement of additional immunoregulatory mechanisms beyond classical checkpoint pathways [[3](https://www.nature.com/articles/s41416-026-03606-8#ref-CR3 "Ferris RL, Blumenschein G Jr., Fayette J, Guigay J, Colevas AD, Licitra L, et al. Nivolumab for recurrent squamous-cell carcinoma of the head and neck. N Engl J Med. 2016;375:1856–67."),[4](https://www.nature.com/articles/s41416-026-03606-8#ref-CR4 "Burtness B, Harrington KJ, Greil R, Soulieres D, Tahara M, de Castro G Jr, et al. Pembrolizumab alone or with chemotherapy versus cetuximab with chemotherapy for recurrent or metastatic squamous cell carcinoma of the head and neck \(KEYNOTE-048\): a randomised, open-label, phase 3 study. Lancet. 2019;394:1915–28."),[5](https://www.nature.com/articles/s41416-026-03606-8#ref-CR5 "Haddad RI, Harrington K, Tahara M, Ferris RL, Gillison M, Fayette J, et al. Nivolumab plus ipilimumab versus EXTREME regimen as first-line treatment for recurrent/metastatic squamous cell carcinoma of the head and neck: The final results of CheckMate 651. J Clin Oncol. 2023;41:2166–80.")]. Tumours release various factors that inhibit immune cell function, including tumour-derived small extracellular vesicles (TEVs). TEVs derived from HNCs have been found to suppress the function of T and B cells [[6](https://www.nature.com/articles/s41416-026-03606-8#ref-CR6 "Ludwig S, Floros T, Theodoraki MN, Hong CS, Jackson EK, Lang S, et al. Suppression of lymphocyte functions by plasma exosomes correlates with disease activity in patients with head and neck cancer. Clin Cancer Res. 2017;23:4843–54."), [7](https://www.nature.com/articles/s41416-026-03606-8#ref-CR7 "Coray M, Goldi V, Schmid L, Benecke L, Figueiro F, Muller L. Differential immunomodulatory effects of head and neck cancer-derived exosomes on B cells in the presence of ATP. Int J Mol Sci. 2022. https://doi.org/10.3390/ijms232214446 .")], reduce the cytotoxicity of natural killer (NK) cells [[6](https://www.nature.com/articles/s41416-026-03606-8#ref-CR6 "Ludwig S, Floros T, Theodoraki MN, Hong CS, Jackson EK, Lang S, et al. Suppression of lymphocyte functions by plasma exosomes correlates with disease activity in patients with head and neck cancer. Clin Cancer Res. 2017;23:4843–54."), [8](https://www.nature.com/articles/s41416-026-03606-8#ref-CR8 "Clayton A, Mitchell JP, Court J, Linnane S, Mason MD, Tabi Z. Human tumor-derived exosomes down-modulate NKG2D expression. J Immunol. 2008;180:7249–58.")], promote a pro-inflammatory phenotype in macrophages [[9](https://www.nature.com/articles/s41416-026-03606-8#ref-CR9 "Tong F, Mao X, Zhang S, Xie H, Yan B, Wang B, et al. HPV + HNSCC-derived exosomal miR-9 induces macrophage M1 polarization and increases tumor radiosensitivity. Cancer Lett. 2020;478:34–44.")], and alter antigen-processing in dendritic cells [[10](https://www.nature.com/articles/s41416-026-03606-8#ref-CR10 "Ludwig S, Sharma P, Theodoraki M.N, Pietrowska M, Yerneni S.S, Lang S, et al. Molecular and functional profiles of exosomes from HPV\(+\) and HPV\(−\) head and neck cancer cell lines. Front Oncol \(2018\). https://doi.org/10.3389/fonc.2018.00445 .")]. Small extracellular vesicles (sEVs) from plasma and saliva of HNC patients promote immunosuppression [[11](https://www.nature.com/articles/s41416-026-03606-8#ref-CR11 "Tengler L, Tiedtke M, Schutz J, Bieback K, Uhlig S, Theodoraki MN, et al. Optimization of extracellular vesicles preparation from saliva of head and neck cancer patients. Sci Rep. 2024. https://doi.org/10.1038/s41598-023-50610-6 ."), [12](https://www.nature.com/articles/s41416-026-03606-8#ref-CR12 "Beccard IJ, Hofmann L, Schroeder JC, Ludwig S, Laban S, Brunner C, et al. Immune suppressive effects of plasma-derived exosome populations in head and neck cancer. Cancers. 2020. https://doi.org/10.3390/cancers12071997 .")], while plasma sEVs also enhance angiogenesis in a stage-dependent manner [[13](https://www.nature.com/articles/s41416-026-03606-8#ref-CR13 "Tengler L, Schutz J, Tiedtke M, Jablonska J, Theodoraki MN, Nitschke K, et al. Plasma-derived small extracellular vesicles unleash the angiogenic potential in head and neck cancer patients. Mol Med. 2023. https://doi.org/10.1186/s10020-023-00659-w .")]. To better understand the role of plasma sEVs in immune evasion and cancer progression, it is important to investigate the alterations occurring in recipient immune cells. Previous studies have demonstrated that plasma sEVs from HNC patients contain elevated levels of immunosuppressive molecules and can significantly impair T-cell functions compared to those from healthy donors [[11](https://www.nature.com/articles/s41416-026-03606-8#ref-CR11 "Tengler L, Tiedtke M, Schutz J, Bieback K, Uhlig S, Theodoraki MN, et al. Optimization of extracellular vesicles preparation from saliva of head and neck cancer patients. Sci Rep. 2024. https://doi.org/10.1038/s41598-023-50610-6 ."), [14](https://www.nature.com/articles/s41416-026-03606-8#ref-CR14 "Schuler PJ, Saze Z, Hong CS, Muller L, Gillespie DG, Cheng D, et al. Human CD4+ CD39+ regulatory T cells produce adenosine upon co-expression of surface CD73 or contact with CD73+ exosomes or CD73+ cells. Clin Exp Immunol. 2014;177:531–43.")]. TEVs carrying PD-L1 and PD-L2, the ligands for PD-1, directly inhibit T-cell activity, promoting tumour immune escape, and mediate resistance to ICIs [[15](https://www.nature.com/articles/s41416-026-03606-8#ref-CR15 "Whiteside TL. Tumor-derived exosomes and their role in cancer progression. Adv Clin Chem. 2016;74:103–41."), [16](https://www.nature.com/articles/s41416-026-03606-8#ref-CR16 "Affolter A, Liebel K, Tengler L, Seiz E, Tiedtke M, Azhakesan A, et al. Modulation of PD‑L1 expression by standard therapy in head and neck cancer cell lines and exosomes. Int J Oncol. 2023. https://doi.org/10.3892/ijo.2023.5550 .")]. Furthermore, the adenosinergic pathway represents an important mechanism through which TEVs exert their immunosuppressive effects [[14](https://www.nature.com/articles/s41416-026-03606-8#ref-CR14 "Schuler PJ, Saze Z, Hong CS, Muller L, Gillespie DG, Cheng D, et al. Human CD4+ CD39+ regulatory T cells produce adenosine upon co-expression of surface CD73 or contact with CD73+ exosomes or CD73+ cells. Clin Exp Immunol. 2014;177:531–43.")]. This pathway, mediated by ectonucleotidases CD39 and CD73, facilitates adenosine, which creates an immunosuppressive environment favouring tumour progression. Recent findings also suggest that TEVs can influence the function of immune cells not only through uptake but also through direct contact, allowing for more efficient modification of several immune cells even after removal of the sEVs [[17](https://www.nature.com/articles/s41416-026-03606-8#ref-CR17 "Muller L, Simms P, Hong CS, Nishimura MI, Jackson EK, Watkins SC, et al. Human tumor-derived exosomes \(TEX\) regulate Treg functions via cell surface signaling rather than uptake mechanisms. Oncoimmunology. 2017. https://doi.org/10.1080/2162402X.2016.1261243 .")]. The aim of the study was to investigate the role of plasma sEVs from HNC patients in immune modulation by examining how these vesicles alter recipient immune cell function and gene expression. By exploring the interactions between sEVs and ICIs, this study aims to contribute to a better understanding of sEV-mediated immune regulation and its possible relevance for tumour immune escape and biomarker development in HNC. ## Methods ### Plasma sample collection Venous blood was collected in citrate monovettes (Sarstedt) from head and neck cancer patients (HNC, _N_ = 50) as well as recovered patients (no evident disease, NED, _N_ = 20) and healthy donors (HD, _N_ = 22) at the Department of Otorhinolaryngology, Head and Neck Surgery of the University Hospital Mannheim from 2019 until 2023. The overall study sample size was determined by sample availability. Detailed information on clinicopathological characteristics is provided in Supplementary Table [1](https://www.nature.com/articles/s41416-026-03606-8#MOESM1). Participant consent was obtained before study inclusion, and the Ethics Committee II of the University of Heidelberg (2021-552 and 2019-697 N) approved the study. For plasma separation, the blood samples were centrifuged at 2000 × _g_ for 10 min at room temperature (RT), aliquoted, and stored at −80 °C. ### sEV isolation To isolate sEVs from patient plasma, size-exclusion chromatography (SEC) was performed as described previously [[18](https://www.nature.com/articles/s41416-026-03606-8#ref-CR18 "Hong CS, Funk S, Muller L, Boyiadzis M, Whiteside TL. Isolation of biologically active and morphologically intact exosomes from plasma of patients with cancer. J Extracell Vesicles. 2016. https://doi.org/10.3402/jev.v5.29289 .")]. Briefly, plasma samples were centrifuged at 2000 × _g_ for 10 min at RT, followed by another centrifugation step at 14,000 × _g_ for 30 min at 4 °C. Subsequently, the plasma was filtered through a 0.22 µm filter (Merck). SEC columns were self-made using 10 mL of cross-linked Sepharose CL-2B (Cytiva) and Econo-Pac columns (Bio-Rad). Next, 1 mL of pre-cleared plasma was applied onto the column bed, and the fourth fraction (1 mL) of PBS eluate was collected. ### Physical characterisation of sEVs Transmission electron microscopy (TEM) of sEVs from two HNC patients
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