. 2025 Nov 26;188(24):6720-6736.e26.

doi: 10.1016/j.cell.2025.09.021. Epub 2025 Oct 17.

CRATER tumor niches facilitate CD8⁺ T cell engagement and correspond with immunotherapy success

Aya Ludin¹, Georgia L Stirtz², Asaf Tal², Ajit J Nirmal³, Kathleen L Pfaff⁴, Michael Manos⁴, Naomi Besson⁴, Nebiyat Eskndir⁴, Billie Porter⁴, Stephanie M Jones⁴, Hannah M Faulkner⁴, Qiyu Gong⁵, Sophia Liu⁶, Irving Barrera⁵, Lijian Wu⁷, Cecilia Pessoa Rodrigues¹, Aditi Sahu⁸, Elizabeth Jerison⁹, Joao V Alessi¹⁰, Biagio Ricciuti¹⁰, Douglas S Richardson¹¹, Jodi D Weiss², Hadley M Moreau², Meredith E Stanhope², Alexander B Afeyan², James Sefton², Wyatt D McCall², Emily Formato¹, Song Yang¹², Yi Zhou¹², David P Hoytema van Konijnenburg¹³, Hannah L Cole², Miguel Cordova⁸, Liang Deng⁸, Milind Rajadhyaksha⁸, Stephen R Quake¹⁴, Mark M Awad¹⁰, Fei Chen¹⁵, Kai W Wucherpfennig⁷, Peter K Sorger¹⁶, F Stephen Hodi¹⁷, Scott J Rodig¹⁸, George F Murphy¹⁹, Leonard I Zon²⁰

Affiliations

¹ Harvard Stem Cell and Regenerative Biology Department, Harvard University, Cambridge, MA 02138, USA; Stem Cell Program and Division of Hematology/Oncology, Boston Children's Hospital, Boston, MA 02115, USA.
² Harvard Stem Cell and Regenerative Biology Department, Harvard University, Cambridge, MA 02138, USA.
³ Department of Dermatology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA; Ludwig Center at Harvard, Boston, MA 02115, USA; Laboratory of Systems Pharmacology, Department of Systems Biology, Harvard Medical School, Boston, MA 02115, USA.
⁴ Center for Immuno-Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA.
⁵ Broad Institute of MIT and Harvard, Cambridge, MA 02139, USA.
⁶ Broad Institute of MIT and Harvard, Cambridge, MA 02139, USA; Ragon Institute of MGH, MIT and Harvard, Cambridge, MA 02139, USA.
⁷ Department of Cancer Immunology and Virology, Dana-Farber Cancer Institute, Boston, MA 02115, USA.
⁸ Dermatology Service, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA.
⁹ Department of Physics, University of Chicago, Chicago, IL 60637, USA.
¹⁰ Lowe Center for Thoracic Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA.
¹¹ Harvard Center for Biological Imaging, Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138, USA.
¹² Stem Cell Program and Division of Hematology/Oncology, Boston Children's Hospital, Boston, MA 02115, USA.
¹³ Division of Immunology, Boston Children's Hospital and Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA.
¹⁴ Department of Bioengineering and Applied Sciences, Stanford University, Stanford, CA 94305, USA; Chan Zuckerberg Biohub, San Francisco, CA 94158, USA.
¹⁵ Harvard Stem Cell and Regenerative Biology Department, Harvard University, Cambridge, MA 02138, USA; Broad Institute of MIT and Harvard, Cambridge, MA 02139, USA.
¹⁶ Ludwig Center at Harvard, Boston, MA 02115, USA; Laboratory of Systems Pharmacology, Department of Systems Biology, Harvard Medical School, Boston, MA 02115, USA.
¹⁷ Center for Immuno-Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA; Parker Institute for Cancer Immunotherapy, Boston, MA, USA.
¹⁸ Center for Immuno-Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA; Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
¹⁹ Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
²⁰ Harvard Stem Cell and Regenerative Biology Department, Harvard University, Cambridge, MA 02138, USA; Stem Cell Program and Division of Hematology/Oncology, Boston Children's Hospital, Boston, MA 02115, USA; Howard Hughes Medical Institute, Harvard Medical School, Boston, MA 02115, USA. Electronic address: leonard.zon@enders.tch.harvard.edu.

PMID: 41109214
PMCID: PMC12604482
DOI: 10.1016/j.cell.2025.09.021

CRATER tumor niches facilitate CD8⁺ T cell engagement and correspond with immunotherapy success

Aya Ludin et al. Cell. 2025.

. 2025 Nov 26;188(24):6720-6736.e26.

doi: 10.1016/j.cell.2025.09.021. Epub 2025 Oct 17.

Authors

Affiliations

¹ Harvard Stem Cell and Regenerative Biology Department, Harvard University, Cambridge, MA 02138, USA; Stem Cell Program and Division of Hematology/Oncology, Boston Children's Hospital, Boston, MA 02115, USA.
² Harvard Stem Cell and Regenerative Biology Department, Harvard University, Cambridge, MA 02138, USA.
³ Department of Dermatology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA; Ludwig Center at Harvard, Boston, MA 02115, USA; Laboratory of Systems Pharmacology, Department of Systems Biology, Harvard Medical School, Boston, MA 02115, USA.
⁴ Center for Immuno-Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA.
⁵ Broad Institute of MIT and Harvard, Cambridge, MA 02139, USA.
⁶ Broad Institute of MIT and Harvard, Cambridge, MA 02139, USA; Ragon Institute of MGH, MIT and Harvard, Cambridge, MA 02139, USA.
⁷ Department of Cancer Immunology and Virology, Dana-Farber Cancer Institute, Boston, MA 02115, USA.
⁸ Dermatology Service, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA.
⁹ Department of Physics, University of Chicago, Chicago, IL 60637, USA.
¹⁰ Lowe Center for Thoracic Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA.
¹¹ Harvard Center for Biological Imaging, Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138, USA.
¹² Stem Cell Program and Division of Hematology/Oncology, Boston Children's Hospital, Boston, MA 02115, USA.
¹³ Division of Immunology, Boston Children's Hospital and Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA.
¹⁴ Department of Bioengineering and Applied Sciences, Stanford University, Stanford, CA 94305, USA; Chan Zuckerberg Biohub, San Francisco, CA 94158, USA.
¹⁵ Harvard Stem Cell and Regenerative Biology Department, Harvard University, Cambridge, MA 02138, USA; Broad Institute of MIT and Harvard, Cambridge, MA 02139, USA.
¹⁶ Ludwig Center at Harvard, Boston, MA 02115, USA; Laboratory of Systems Pharmacology, Department of Systems Biology, Harvard Medical School, Boston, MA 02115, USA.
¹⁷ Center for Immuno-Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA; Parker Institute for Cancer Immunotherapy, Boston, MA, USA.
¹⁸ Center for Immuno-Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA; Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
¹⁹ Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
²⁰ Harvard Stem Cell and Regenerative Biology Department, Harvard University, Cambridge, MA 02138, USA; Stem Cell Program and Division of Hematology/Oncology, Boston Children's Hospital, Boston, MA 02115, USA; Howard Hughes Medical Institute, Harvard Medical School, Boston, MA 02115, USA. Electronic address: leonard.zon@enders.tch.harvard.edu.

PMID: 41109214
PMCID: PMC12604482
DOI: 10.1016/j.cell.2025.09.021

Abstract

T cell-mediated tumor killing underlies immunotherapy success. Here, we used long-term in vivo imaging and high-resolution spatial transcriptomics of zebrafish endogenous melanoma, as well as multiplex imaging of human melanoma, to identify domains facilitating the immune response during immunotherapy. We identified cancer regions of antigen presentation and T cell engagement and retention (CRATERs) as pockets at the stroma-melanocyte boundaries of zebrafish and human melanoma. CRATERs are rich in antigen-recognition molecules, harboring the highest density of CD8⁺ T cells in tumors. In zebrafish, CD8⁺ T cells formed prolonged interactions with melanoma cells within CRATERs, characteristic of antigen recognition. Following immunostimulatory treatment, CRATERs expanded, becoming the major sites of activated CD8⁺ T cell accumulation and tumor killing. In humans, elevation in CRATER density in biopsies following immune checkpoint blockade (ICB) therapy correlated with a clinical response to therapy. CRATERs are structures that show active tumor killing and may be useful as a diagnostic indicator for immunotherapy success.

Keywords: CD8+ T cells; cancer; immune response; immunotherapy; melanoma; zebrafish.

PubMed Disclaimer

Conflict of interest statement

Declaration of interests L.I.Z. is a founder and stockholder of Fate Therapeutics, CAMP4 Therapeutics, Amagma Therapeutics, Scholar Rock, and Branch Biosciences and a consultant for Celularity and Cellarity. F.S.H. reports grants and personal fees related to the submitted work from Bristol-Myers Squibb and Novartis and personal fees from Merck, Surface, Compass Therapeutics, Apricity, 7 Hills Pharma, Bicara, Checkpoint Therapeutics, Bioentre, Gossamer, Iovance, Catalym, Immunocore, Kairos, Rheos, Zumutor, Corner Therapeuitcs, Puretech, Curis, Astra Zeneca, and Solu Therapeutics. Outside the submitted work, F.S.H. has the following patents: Methods for Treating MICA-Related Disorders (#20100111973) with royalties paid; Tumor antigens and uses thereof (#7250291) (issued); Angiopoiten-2 Biomarkers Predictive of Anti-immune checkpoint response (#20170248603) (pending); Compositions and Methods for Identification, Assessment, Prevention, and Treatment of Melanoma using PD-L1 Isoforms (#20160340407) (pending); Therapeutic peptides (#20160046716) (pending); Therapeutic Peptides (#20140004112) (pending); Therapeutic Peptides (#20170022275) (pending); Therapeutic Peptides (#20170008962) (pending); THERAPEUTIC PEPTIDES (#9402905) (issued); METHODS OF USING PEMBROLIZUMAB AND TREBANANIB (pending); Vaccine compositions and methods for restoring NKG2D pathway function against cancers (#10279021) (issued); Antibodies that bind to MHC class I polypeptide-related Sequence A (#10106611) (issued); ANTI-GALECTIN ANTIBODY BIOMARKERS PREDICTIVE OF ANTI-IMMUNE CHECKPOINT AND ANTI-ANGIOGENESIS RESPONSES (#20170343552) (pending); and Antibodies against EDIL3 and methods of use thereof (pending). J.V.A. is on the advisory board of BMS and AstraZeneca and consultant for MSD, Janssen. K.W.W. serves on the scientific advisory boards of DEM BioPharma, Solu Therapeutics, D2M Biotherapeutics, DoriNano, Inc., and Nextechinvest. He is a co-founder of Immunitas Therapeutics and receives sponsored research funding from Fate Therapeutics. He holds equity in TScan Therapeutics. These activities are not related to the research reported in this publication.

Figures

**Figure 1.. CD8⁺ T cells preferentially locate in CRATERs on the melanoma surface**
(A) Longitudinal imaging of a mitfa:BFP tumor across stages of development in a Tg(cd8a:EGFP;lck:mCherry) fish. Dashed white lines: scale edges. Left: radial growth of melanoma below the scale. Middle: same tumor after 1 week. Right: same tumor after 3 weeks. Area in rectangle enlarged. Yellow dashed lines: CRATERs. (B) 3D projection of a melanoma tumor in a Tg(cd8α:EGFP) zebrafish (representative of over 100 tumors). Arrows: CD8⁺ T cells. White dashed lines: CRATERs. (C) CD8⁺ cell density (cells per mm²) in CRATER vs. tumor area (n = 5 fish, whiskers represent 1.5× the interquartile range. Mann-Whitney U test, *p value = 0.015). (D) CRATER diameter size (μm) distribution in untreated tumors (n = 3 fish/265 CRATERs). (E) Snapshots from time-lapse imaging of area at rectangle in (B). Dashed line: CRATER. Time is h:min. (F) CRATER at tumor-infiltrated scale edge. Dashed line: scale edge. Time is hours:minutes. (G) Representative 3D image of a tumor in Tg(cd8α:EGFP; fli1a:dsRed) zebrafish. Rectangle areas: enlarged to the right. Dashed lines: CRATERs. White arrows: CD8⁺ T cells. CRATERs emerge adjacent to the fli1a⁺ blood vessel. CD8⁺ T cells interacting with: (1) blood vessels and (2) tumor cells. (H) Number of CRATERs at distances from fli⁺ blood vessels (n = 3 fish, 630 CRATERs). See also Figures S1 and S2.

**Figure 2.. CRATERs are sites of elevated *b2m* expression that retain CD8⁺ T cells in them**
(A) Left: Slide-seq gene expression map of zebrafish melanoma tumor. Black circles: CRATER areas. Dashed black circles: non-CRATER areas. T cells that have entered the tumor can also be noted. Right: rectangle areas, enlarged, showing CRATER and non-CRATER areas. (B) Differential gene expression in CRATER vs. non-CRATER-associated *mitfa*⁺ areas. (C) CD8⁺ cell density in CRATER/non-CRATER tumor surface, in WT and melanocyte-specific B2M-depleted tumors. (Image quantification. n fish = control-4, B2M KO-9. Whiskers represent 1.5× the interquartile range. t test. *p value = 0.003). (D) 3D representative image of B2M intact (control) vs. depleted melanoma. White dashed line: CRATERs. See also Figure S4.

**Figure 3.. Activated CD8⁺ T cells aggregate in CRATERs following CpG ODN immune stimulation**
(A) CRATER coverage in untreated, PBS-, and CpG ODN-injected WT and melanocyte-specific B2M KO, post 4 daily injections. (n fish = UT-5, PBS-5, CpG ODN-5, B2M KO CpG ODN-4. Whiskers represent 1.5× the interquartile range. Mann-Whitney U test, *p value = 0.031, ns = 0.42). (B) CD8⁺ T cell density in CRATERs vs. non-CRATER tumor surface in WT and B2M melanocyte-specific KO tumors, post 4 CpG ODN daily injections (n fish = WT-5, B2M KO-3. Mean ± SE. Mann-Whitney U test, **p value = 0.007). (C) 3D imaging of melanoma tumors in Tg(cd8α: EGFP) fish after four daily intratumoral injections of PBS or CpG ODN, 24 h post last injection, injected into either B2M WT or KO tumors. Arrows: CRATERs. (D) Percents of ifng mRNA expressing cd8a⁺ cells among total cd8⁺ cells within CRATERs or tumor. (n = CpG ODN-4, PBS-3. Mean ± SE. t test. *p value = 0.004). (E) RNAscope staining for mCherry, cd8a, and ifng mRNA following four daily injections of PBS or CpG ODN. Dashed white line: tumor surface. Yellow dashed line: CRATER. Arrows: CD8a⁺ cells. (F) infg mRNA expression detected by RNAscope in cells in CRATERs, tumor border (0–50 um from tumor surface) and within the tumor (n fish = CpG ODN-4, PBS-3. Mean ± SE. **p value = 0.002, *p value = 0.018). See also Figure S3.

**Figure 4.. CRATERs are sites of tumor killing and are remodeled by T cells**
(A) Three examples of CRATERs in 3D confocal images of whole-mount TUNEL assay, in PBS- or CPG ODN-injected tumors (four times daily), WT or melanocyte-specific B2M KO. (B) TUNEL⁺ cell density in CRATERs and non-CRATER tumor area. (Image quantification. n = PBS WT-3 fields of view [FOV] from 3 fish, CpG ODN WT-12 FOV from 8 fish, CpG ODN B2M KO-5 FOV from 2 fish. Whiskers represent 1.5× the interquartile range. t test. p values: *PBS vs. CpG ODN WT = 0.03, **CPG ODN: CRATER vs. tumor = 0.005, **CpG ODN: WT vs. B2M KO = 0.007). (C) 3D imaging of whole-mount TUNEL staining of CpG ODN-treated tumor. White dashed lines: CRATER. Rectangle area enlarged. Image slightly rotated. (D) CRATER coverage in tumors of cd8α:EGFP (WT), cd8α:EGFP;prkdc^−/−, or jak3^−/− transgenic fish (n fish = WT-5, prkdc^(−/−)-2, jak3^(−/−)-3 fish. Mean ± SE. t test, p values: *WT/cd8a:EGFP;prkdc^(−/−) = 0.011, * WT/jak3^(−/−) = 0.01). (E) Representative 3D confocal images of melanoma in WT Tg(cd8a:EGFP) and Tg(cd8a:EGFP;prkdc^(−/−)) fish. Arrows: CD8⁺ T cells. See also Figure S3.

**Figure 5.. CRATERs are found in human melanoma, extending from the tumor margins**
(A) Left: mIF image of a (PVA) within a cutaneous melanoma tumor. Red lines: CRATERs. Yellow line: PMB. Right: rectangle area enlarged. Upper image: collagen fibers lining the CRATERs. Lower image: CD8⁺ T cells within CRATERs. (B) CD105 expression in perivascular area (yellow line) but not in the CRATER (red line). Representative image of 13 melanoma samples. (C) CD8⁺ T cell density in CRATERs, tumor margins (PMB), and embedded in the S100a⁺ tumor mass (within tumor). (n = 2 tumors, 714 CRATERs. Mean ± SE, t test, p values: **CRATER/border = 0.008, **CRATER/tumor = 0.005, *0.023). (D) Mean number of cells per CRATER for each cell type (n = 714 CRATERs, mean ± SE). (E) Representative CyCIF image showing location of CD8⁺ T cells, CD163⁺ DCs, CD4⁺ cells, CD4⁺/FOXP3⁺ T regulatory cells, and CD8⁺/GzmB⁺ cytotoxic T cells at the perivascular and CRATER areas. Abbreviations: BV, blood vessel; PVA, perivascular area; PMB, perivascular-melanocytes boundary; CTL, cytotoxic T cells; Treg, T regulatory cells; GzmB, granzyme B; DCs, dendritic cells (CD11c⁺). See also Figures S5 and S6.

**Figure 6.. CRATERs in human melanoma are sites of high antigen presentation molecules and PD-L1 expression**
(A) Signal intensity distribution of HLA-A staining in S100a⁺ melanoma cells in CRATERs compared with elsewhere in the tumor (“Out”) (n = 2 tumors, 714 CRATERs. Whiskers represent 1.5× the interquartile range. Mann-Whitney U test. ***p value < 0.001). (B) Representative image presenting HLA-A staining in CRATER (dashed white line). Yellow asterisks: melanoma cells lining the CRATER. White asterisks: melanoma cells located away from the CRATER. (C) Signal intensity distribution of HLA-A, MART-1, and HLA-DPB1 staining in CD163⁺/CD11c⁺ DCs in CRATERs compared with elsewhere in the tumor (“Out”) (n = 2 tumors, 714 CRATERs, whiskers represent 1.5× the interquartile range. Mann-Whitney U test, ***p value < 0.001) (D) Representative image of CRATER (white dashed line), stained for CD163⁺ HLA-A, MART-1, and HLADPB1. (E) Signal intensity distribution of PD-L1 staining in CD163⁺/CD11c⁺ DCs in CRATERs compared with elsewhere in the tumor (“Out”) (n = 2 tumors, 714 CRATERs. Whiskers represent 1.5× the interquartile range. Mann-Whitney U test, ***p value < 0.001). (F) Upper: low magnification of a tumor area. High PD-L1 staining within CRATERs. White arrows: CRATERs. Lower: rectangle area enlarged, showing a CRATER (dashed white line) containing PD-L1⁺/CD163⁺/CD11c⁺ DCs. Teal arrows: CD163⁺/CD11c⁺ DCs (with low PD-L1 staining) outside the CRATER. Orange arrows: CD163⁺CD11c⁺ (PD-L1⁺) DCs inside the CRATER. All images and quantifications are CyCIF data.

**Figure 7.. CRATER density is increased following successful ICB treatment**
(A) CRATER linear density (number per cm PMB) in post ICB treatment patients’ samples (n = 4 responders [SD, CR], 9 non-responders [PD]. Whiskers represent 1.5× the interquartile range. t test. *p value = 0.0027). Black dots: metastatic setting. Red dot: T-VEC. Blue dot: neoadjuvant setting. (B) CRATER linear density in pre- and posttreatment samples from the same patient, showing altogether three responders and three non-responders. Each line represents a patient. Dashed line: T-VEC treated. (C) Representative images of mIF-stained samples from a responder and a non-responder. Top: low-magnification view of the sample. Bottom: rectangles enlarged. Yellow lines: PMB. Red lines: CRATERs. (D) mIF for melanoma, CD8, apoptotic cells (activated cas3), and CD105 of biopsies taken before and after treatment from the same patient, who presented SD post treatment (#13 in Table S1). Top images: low-magnification view. Bottom images: rectangles in the respective top image, enlarged. (E) mIF image of biopsy taken during neoadjuvant treatment that presented CR. Left: low-magnification image. Yellow arrows: CRATERs. Right: rectangle areas, enlarged. See also Figure S7.

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Craters on the melanoma surface facilitate tumor-immune interactions and demonstrate pathologic response to checkpoint blockade in humans.
Ludin A, Stirtz GL, Tal A, Nirmal AJ, Besson N, Jones SM, Pfaff KL, Manos M, Liu S, Barrera I, Gong Q, Rodrigues CP, Sahu A, Jerison E, Alessi JV, Ricciuti B, Richardson DS, Weiss JD, Moreau HM, Stanhope ME, Afeyan AB, Sefton J, McCall WD, Formato E, Yang S, Zhou Y, van Konijnenburg DPH, Cole HL, Cordova M, Deng L, Rajadhyaksha M, Quake SR, Awad MM, Chen F, Sorger PK, Hodi FS, Rodig SJ, Murphy GF, Zon LI. Ludin A, et al. bioRxiv [Preprint]. 2024 Sep 19:2024.09.18.613595. doi: 10.1101/2024.09.18.613595. bioRxiv. 2024. Update in: Cell. 2025 Nov 26;188(24):6720-6736.e26. doi: 10.1016/j.cell.2025.09.021. PMID: 39345527 Free PMC article. Updated. Preprint.

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CRATER tumor niches facilitate CD8⁺ T cell engagement and correspond with immunotherapy success

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CRATER tumor niches facilitate CD8⁺ T cell engagement and correspond with immunotherapy success

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