---
title: "CHL1+ immunomodulatory CAFs recruit CXCR3+ regulatory T cells to suppress immunity in lung adenoca"
id: "nature-immunology-1-a-novel-caf-population-coordinates-hyper-suppressive-regulatory-t-cell"
canonical_url: "https://medichelpline.com/clinical-feed/nature-immunology-1-a-novel-caf-population-coordinates-hyper-suppressive-regulatory-t-cell"
content_type: "clinical_feed_article"
specialty: "Infectious Disease"
source_name: "Nature Immunology"
source_url: "https://www.nature.com/articles/s41590-026-02607-2"
published_at: "2026-08-11T10:38:32.000Z"
evidence_level: "Journal Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# CHL1+ immunomodulatory CAFs recruit CXCR3+ regulatory T cells to suppress immunity in lung adenoca
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/nature-immunology-1-a-novel-caf-population-coordinates-hyper-suppressive-regulatory-t-cell
- **Specialty:** [Infectious Disease](https://medichelpline.com/clinical-feed/infectious-disease.md)
- **Primary Source:** Nature Immunology
- **Source URL:** [Original Journal Publication](https://www.nature.com/articles/s41590-026-02607-2)
- **Published At:** 2026-08-11T10:38:32.000Z
- **Evidence Rating:** Journal Feed
## Executive GIST (TL;DR)
- The study identifies a previously undescribed population of cancer-associated fibroblasts in lung adenocarcinoma, termed **imCAFs**, that are defined by high CHL1 expression and an immunomodulatory transcriptional program. - imCAFs are enriched in tumor-associated lung tissue, localize to the tumor border, and are distinct from canonical myofibroblastic CAFs. - Single-cell and spatial transcriptomics show imCAFs colocalize with T cells in the peritumoral region, with a particularly strong spatial association to **FOXP3+ regulatory T (T reg)** cells. - imCAFs express chemokines including **Cxcl9** and **Cxcl10**, with CXCL9 prominently produced by CHL1+ imCAFs and correlating with local T reg cell abundance. - Tumor-infiltrating T reg cells preferentially migrate toward CXCL9 gradients and exhibit higher proliferation and suppressive markers compared with non-tumor T reg cells. - CXCR3 is the receptor for CXCL9; CXCR3+ T reg cells constitute a hyper-suppressive subset that accumulates at tumor borders and is transcriptionally distinct from CXCR3− T reg cells. - Genetic deletion of Cxcr3 in T reg cells or Cxcl9 in stromal cells reduces T reg cell accumulation, increases CD8+ T cell activation and decreases tumor burden in mouse models (details reported in source). - Analogous CHL1+ imCAF-like fibroblasts are present in human non-small cell lung cancer; higher CHL1 expression associates with reduced cytotoxicity and shorter progression-free survival. - The findings highlight an **imCAF–CXCL9–CXCR3+ T reg** axis as a stromal mechanism that coordinates an immunosuppressive tumor microenvironment and a potential therapeutic target in lung cancer.
## Clinical Analysis & Structured Key Points
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[nature](https://www.nature.com/) 2. [nature immunology](https://www.nature.com/ni) 3. [articles](https://www.nature.com/ni/articles?type=article) 4. article A novel CAF population coordinates hyper-suppressive regulatory T cell recruitment and localization in lung cancer [ Download PDF ](https://www.nature.com/articles/s41590-026-02607-2.pdf) [ Download PDF ](https://www.nature.com/articles/s41590-026-02607-2.pdf) * Article * [Open access](https://www.springernature.com/gp/open-science/about/the-fundamentals-of-open-access-and-open-research) * Published: 11 August 2026 # A novel CAF population coordinates hyper-suppressive regulatory T cell recruitment and localization in lung cancer * [Olivia R. Ringham](https://www.nature.com/articles/s41590-026-02607-2#auth-Olivia_R_-Ringham-Aff1-Aff2)[1](https://www.nature.com/articles/s41590-026-02607-2#Aff1),[2](https://www.nature.com/articles/s41590-026-02607-2#Aff2), * [Monica Rivera](https://www.nature.com/articles/s41590-026-02607-2#auth-Monica-Rivera-Aff1)[1](https://www.nature.com/articles/s41590-026-02607-2#Aff1), * [Lucas F. Loffredo](https://www.nature.com/articles/s41590-026-02607-2#auth-Lucas_F_-Loffredo-Aff1)[1](https://www.nature.com/articles/s41590-026-02607-2#Aff1), * [Melih Arda Ozsoy](https://www.nature.com/articles/s41590-026-02607-2#auth-Melih_Arda-Ozsoy-Aff1)[1](https://www.nature.com/articles/s41590-026-02607-2#Aff1), * [Christina M. Healy](https://www.nature.com/articles/s41590-026-02607-2#auth-Christina_M_-Healy-Aff1)[1](https://www.nature.com/articles/s41590-026-02607-2#Aff1), * [Maye F. Cheng](https://www.nature.com/articles/s41590-026-02607-2#auth-Maye_F_-Cheng-Aff3)[3](https://www.nature.com/articles/s41590-026-02607-2#Aff3), * [Yinuo Jin](https://www.nature.com/articles/s41590-026-02607-2#auth-Yinuo-Jin-Aff4)[4](https://www.nature.com/articles/s41590-026-02607-2#Aff4), * [Noah Chen](https://www.nature.com/articles/s41590-026-02607-2#auth-Noah-Chen-Aff1-Aff2)[1](https://www.nature.com/articles/s41590-026-02607-2#Aff1),[2](https://www.nature.com/articles/s41590-026-02607-2#Aff2), * [Kenia de los Santos-Alexis](https://www.nature.com/articles/s41590-026-02607-2#auth-Kenia-Santos_Alexis-Aff1)[1](https://www.nature.com/articles/s41590-026-02607-2#Aff1), * [Elham Azizi](https://www.nature.com/articles/s41590-026-02607-2#auth-Elham-Azizi-Aff4-Aff5)[4](https://www.nature.com/articles/s41590-026-02607-2#Aff4),[5](https://www.nature.com/articles/s41590-026-02607-2#Aff5), * [Anjali Saqi](https://www.nature.com/articles/s41590-026-02607-2#auth-Anjali-Saqi-Aff6)[6](https://www.nature.com/articles/s41590-026-02607-2#Aff6), * [Matthew B. Buechler](https://www.nature.com/articles/s41590-026-02607-2#auth-Matthew_B_-Buechler-Aff3) [ORCID: orcid.org/0000-0003-1902-622X](https://orcid.org/0000-0003-1902-622X)[3](https://www.nature.com/articles/s41590-026-02607-2#Aff3), * [Carla P. Concepcion-Crisol](https://www.nature.com/articles/s41590-026-02607-2#auth-Carla_P_-Concepcion_Crisol-Aff2)[2](https://www.nature.com/articles/s41590-026-02607-2#Aff2) & * … * [Nicholas Arpaia](https://www.nature.com/articles/s41590-026-02607-2#auth-Nicholas-Arpaia-Aff1-Aff2) [ORCID: orcid.org/0000-0002-0657-0528](https://orcid.org/0000-0002-0657-0528)[1](https://www.nature.com/articles/s41590-026-02607-2#Aff1),[2](https://www.nature.com/articles/s41590-026-02607-2#Aff2) Show authors [_Nature Immunology_](https://www.nature.com/ni) (2026) [Cite this article](https://www.nature.com/articles/s41590-026-02607-2#citeas) [ Save article ](https://www.nature.com/articles/s41590-026-02607-2/save-research?_csrf=6U7NBQ4_yk0-8mr3M5owOIAn_wgUrHyi) [ View saved research ](https://www.nature.com/saved-research) ## Abstract Across many solid tumor types, cancer-associated fibroblasts (CAFs) are abundant and heterogeneous, with distinct subpopulations exerting immunomodulatory functions. Here we identify a novel population of immunomodulatory CAFs (imCAFs) in primary lung adenocarcinoma and pulmonary metastases, characterized by cell adhesion molecule L1-like (CHL1) expression and enriched in immune regulation and chemokine signaling programs. Through single-cell and spatial transcriptomics, we demonstrate that imCAFs are spatially colocalized with CXCR3+ regulatory T (Treg) cells, a hyper-suppressive subset accumulating at the tumor border. imCAFs produce CXCL9, driving CXCR3+ Treg cell recruitment and promoting an immunosuppressive microenvironment. CXCR3+ Treg cells display enhanced proliferative and suppressive capacity and are transcriptionally distinct from CXCR3− counterparts. Genetic ablation of _Cxcr3_ in Treg cells or _Cxcl9_ in stromal cells reduces Treg cell accumulation, enhances CD8+ T cell activation and decreases tumor burden. Analogous CHL1+ imCAF-like fibroblasts in human non-small cell lung cancer colocalize with Treg cells, and elevated _CHL1_ expression is associated with reduced cytotoxicity and decreased progression-free survival, highlighting the imCAF–CXCL9–CXCR3+ Treg axis as a promising therapeutic target. ## Main The tumor microenvironment (TME) is a highly complex multicellular network that plays a central role in dictating tumor progression and response to anticancer therapy. Solid tumors often exhibit desmoplastic features, which are characterized by the presence of activated CAFs. Rather than a uniform entity, CAFs encompass distinct subpopulations, with specialized roles in tumor progression, extracellular matrix remodeling and immune modulation[1](https://www.nature.com/articles/s41590-026-02607-2#ref-CR1 "Cords, L. et al. Cancer-associated fibroblast phenotypes are associated with patient outcome in non-small cell lung cancer. Cancer Cell 42, 396–412 \(2024\)."),[2](https://www.nature.com/articles/s41590-026-02607-2#ref-CR2 "Louault, K., Li, R. R. & DeClerck, Y. A. Cancer-associated fibroblasts: understanding their heterogeneity. Cancers 12, 3108 \(2020\)."). Among these, immune-interacting CAFs represent a particularly important and functionally unique CAF niche found across various malagnancies[3](https://www.nature.com/articles/s41590-026-02607-2#ref-CR3 "Mhaidly, R. & Mechta-Grigoriou, F. Role of cancer-associated fibroblast subpopulations in immune infiltration, as a new means of treatment in cancer. Immunol. Rev. 302, 259–272 \(2021\)."). In highly desmoplastic cancers, such as pancreatic ductal adenocarcinoma (PDAC), liver cancers and breast cancers, immune-interacting subpopulations of CAFs have been shown to regulate lymphocyte activation, recruitment and retention, and serve as key markers of prognosis and overall survival[4](https://www.nature.com/articles/s41590-026-02607-2#ref-CR4 "Song, M. et al. Cancer-associated fibroblast-mediated cellular crosstalk supports hepatocellular carcinoma progression. Hepatology 73, 1717–1735 \(2021\)."),[5](https://www.nature.com/articles/s41590-026-02607-2#ref-CR5 "Costa, A. et al. Fibroblast heterogeneity and immunosuppressive environment in human breast cancer. Cancer Cell 33, 463–479 \(2018\)."),[6](https://www.nature.com/articles/s41590-026-02607-2#ref-CR6 "Ohlund, D. et al. Distinct populations of inflammatory fibroblasts and myofibroblasts in pancreatic cancer. J. Exp. Med. 214, 579–596 \(2017\)."),[7](https://www.nature.com/articles/s41590-026-02607-2#ref-CR7 "Huang, H. et al. Mesothelial cell-derived antigen-presenting cancer-associated fibroblasts induce expansion of regulatory T cells in pancreatic cancer. Cancer Cell 40, 656–673 \(2022\)."). However, CAF subtypes and their impact on immune coordination in other solid tumors, such as lung adenocarcinoma (LUAD), remain less characterized. Lung cancer remains the leading cause of cancer-related mortality in the United States, with adenocarcinoma as the most prevalent form[8](https://www.nature.com/articles/s41590-026-02607-2#ref-CR8 "Herbst, R. S., Morgensztern, D. & Boshoff, C. The biology and management of non-small cell lung cancer. Nature 553, 446–454 \(2018\)."). Importantly, invasive LUAD commonly manifests in solid tumors that are poised to form a rich desmoplastic microenvironment. The lung is also among the most frequent sites of metastasis for many cancers, with up to half of metastatic colonization events forming solid tumors in this organ[9](https://www.nature.com/articles/s41590-026-02607-2#ref-CR9 "Xiao, G., Wang, X., Xu, Z., Liu, Y. & Jing, J. Lung-specific metastasis: the coevolution of tumor cells and lung microenvironment. Mol. Cancer 24, 118 \(2025\)."). Evidence of stage-dependent immune cell infiltration in LUAD[10](https://www.nature.com/articles/s41590-026-02607-2#ref-CR10 "Banat, G. A. et al. Immune and inflammatory cell composition of human lung cancer stroma. PLoS ONE 10, e0139073 \(2015\).") suggests that dynamic niches within the TME regulate antitumor immunity and influence tumor progression. Moreover, fibroblast niches within lung tumor stroma have been shown to express high levels of regulatory surface molecules, cytokines and chemokines that are canonically known to alter the functions of tumor-infiltrating lymphocytes[10](https://www.nature.com/articles/s41590-026-02607-2#ref-CR10 "Banat, G. A. et al. Immune and inflammatory cell composition of human lung cancer stroma. PLoS ONE 10, e0139073 \(2015\)."),[11](https://www.nature.com/articles/s41590-026-02607-2#ref-CR11 "Kerdidani, D. et al. Lung tumor MHCII immunity depends on in situ antigen presentation by fibroblasts. J. Exp. Med. 219, e20210815 \(2022\)."),[12](https://www.nature.com/articles/s41590-026-02607-2#ref-CR12 "Cheng, H. W. et al. CCL19-producing fibroblastic stromal cells restrain lung carcinoma growth by promoting local antitumor T-cell responses. J. Allergy Clin. Immunol. 142, 1257–1271 \(2018\)."),[13](https://www.nature.com/articles/s41590-026-02607-2#ref-CR13 "Grout, J. A. et al. Spatial positioning and matrix programs of cancer-associated fibroblasts promote T-cell exclusion in human lung tumors. Cancer Discov. 12, 2606–2625 \(2022\)."). Characterization of CAF populations in human lung cancers demonstrates that the presence and spatial distribution of distinct immune-modulating CAFs is a strong independent prognostic factor for patient survival[1](https://www.nature.com/articles/s41590-026-02607-2#ref-CR1 "Cords, L. et al. Cancer-associated fibroblast phenotypes are associated with patient outcome in non-small cell lung cancer. Cancer Cell 42, 396–412 \(2024\)."),[14](https://www.nature.com/articles/s41590-026-02607-2#ref-CR14 "Hanley, C. J. et al. Single-cell analysis reveals prognostic fibroblast subpopulations linked to molecular and immunological subtypes of lung cancer. Nat. Commun. 14, 387 \(2023\)."), which can influence the tumor–immune microenvironment and response to cancer treatments[15](https://www.nature.com/articles/s41590-026-02607-2#ref-CR15 "Hu, H. et al. Three subtypes of lung cancer fibroblasts define distinct therapeutic paradigms. Cancer Cell 39, 1531–1547 \(2021\)."). However, few studies have aimed to identify the ontogeny of distinct immune-interacting CAF populations or investigate the mechanisms by which CAFs modulate pro-tumor versus antitumor immune responses. Although many leukocytes act to influence the immune landscape of lung tumors, Treg cells play a particularly critical role in promoting tumor progression by dampening antitumor immunity[16](https://www.nature.com/articles/s41590-026-02607-2#ref-CR16 "Tay, C., Tanaka, A. & Sakaguchi, S. Tumor-infiltrating regulatory T cells as targets of cancer immunotherapy. Cancer Cell 41, 450–465 \(2023\)."). Recently, several studies have suggested a role for distinct CAF populations in influencing Treg cell dynamics and function in the TME of various solid tumor malignancies. In melanoma, breast and ovarian cancers, the presence of specific CAF subtypes has been correlated with enhanced Treg cell trafficking, retention and activation in the TME, likely through chemokine signaling gradients and specialized receptor–ligand interactions[5](https://www.nature.com/articles/s41590-026-02607-2#ref-CR5 "Costa, A. et al. Fibroblast heterogeneity and immunosuppressive environment in human breast cancer. Cancer Cell 33, 463–479 \(2018\)."),[17](https://www.nature.com/articles/s41590-026-02607-2#ref-CR17 "Givel, A. M. et al. miR200-regulated CXCL12beta promotes fibroblast heterogeneity and immunosuppression in ovarian cancers. Nat. Commun. 9, 1056 \(2018\)."),[18](https://www.nature.com/articles/s41590-026-02607-2#ref-CR18 "Varveri, A. et al. Immunological synapse formation between T regulatory cells and cancer-associated fibroblasts promotes tumour development. Nat. Commun. 15, 4988 \(2024\)."). In patients with LUAD, Treg cells preferentially localize within the tumor stroma, and their increased presence correlates with significantly poorer prognosis[19](https://www.nature.com/articles/s41590-026-02607-2#ref-CR19 "Kinoshita, T. et al. Forkhead box P3 regulatory T cells coexisting with cancer associated fibroblasts are correlated with a poor outcome in lung adenocarcinoma. Cancer Sci. 104, 409–415 \(2013\)."). However, the underlying mechanisms by which distinct CAF subsets modulate Treg cell dynamics in lung tumors remain poorly understood. In this report, we identify a population of imCAFs that play a pivotal role in shaping the lung TME by driving the recruitment of a highly immunosuppressive subset of CXCR3+ Treg cells. Through the CXCL9–CXCR3 axis, imCAFs influence Treg cell localization, activation and function, ultimately promoting an immunosuppressive TME and resulting in increased tumor burden in mouse models, with similar prognostic associations observed in humans. These results provide critical insights into the interplay between stromal and immune compartments in LUAD and suggest that targeting the imCAF–Treg cell axis may represent a promising therapeutic avenue for improving antitumor immune responses in patients with lung cancer. ## Results ### imCAFs are enriched in lung tumor tissue To identify phenotypically and functionally distinct populations of CAFs within the lung TME, we intravenously injected mice with GFP-expressing Lewis lung carcinoma (LLCGFP) cells—an orthotopic model of LUAD—and performed single-cell RNA sequencing (scRNA-seq) on fluorescence-activated cell sorting (FACS)-sorted PDGFRα+ fibroblasts isolated from lung tumor tissue and normal-adjacent lung tissue (gating strategy in Supplementary Fig. [1a](https://www.nature.com/articles/s41590-026-02607-2#MOESM1)). Utilizing this transcriptomic approach, we uncovered seven transcriptionally distinct clusters of fibroblasts (Fig. [1a,b](https://www.nature.com/articles/s41590-026-02607-2#Fig1)). We used hallmark genes to ascribe functional identities to most clusters, such as _Col14a1_ + fibroblasts[20](https://www.nature.com/articles/s41590-026-02607-2#ref-CR20 "Kaiser, K. A., Loffredo, L. F., Santos-Alexis, K. L., Ringham, O. R. & Arpaia, N. Regulation of the alveolar regenerative niche by amphiregulin-producing regulatory T cells. J. Exp. Med. 220, e20221462 \(2023\)."), _Scube2_ + alveolar fibroblasts[21](https://www.nature.com/articles/s41590-026-02607-2#ref-CR21 "Tsukui, T., Wolters, P. J. & Sheppard, D. Alveolar fibroblast lineage orchestrates lung inflammation and fibrosis. Nature 631, 627–634 \(2024\)."), _Pi16_ + adventitial fibroblasts[22](https://www.nature.com/articles/s41590-026-02607-2#ref-CR22 "Buechler, M. B. et al. Cross-tissue organization of the fibroblast linea
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