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Correction: B cell tolerance and antibody production to the celiac disease autoantigen transglutaminase 2

M. Fleur du Pré, Jana Blazevski, Alisa E. Dewan, Jorunn Stamnaes, Chakravarthi Kanduri, Geir Kjetil Sandve, Marie K. Johannesen, Christian B. Lindstad, Kathrin Hnida, Lars Fugger, Gerry Melino, Shuo-Wang Qiao, Ludvig M. Sollid

J Exp Med (2026) 223 (3): e2019086002062026c.

https://doi.org/10.1084/jem.2019086002062026c

Published: 12 February 2026

View article titled, Correction: B cell tolerance and antibody production to the celiac disease autoantigen transglutaminase 2

Journal Articles

Correction: Contribution of IL-17–producing γδ T cells to the efficacy of anticancer chemotherapy

J Exp Med (2026) 223 (3): e2010026902032026c.

https://doi.org/10.1084/jem.2010026902032026c

Published: 12 February 2026

View article titled, Correction: Contribution of IL-17–producing γδ T cells to the efficacy of anticancer chemotherapy

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Untitled image

in Correction: Contribution of IL-17–producing γδ T cells to the efficacy of anticancer chemotherapy > Journal of Experimental Medicine

Published: 12 February 2026

More about this image found in Untitled image

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Vγ chain usage by γδ T17 cells in tumor bed and skin draining LNs of naive mice. (A) CD45, CD3, CD4, and TCR δ expression by IL-17A–producing cells from tumor beds of mice 8 d after chemotherapy. (B) Vγ usage in live CD45+ CD3+ TCR δ+ IL-17+ cells in tumor beds after DX. Numbers represent the percentage of Vγ1+, Vγ4+, or Vγ7+ cells among TCR δ+ IL-17+ cells as indicated. One experiment representative of three is shown. (C–E) Individual Vγ1−Vγ4−Vγ7− γδ T17 TILs as gated in (C) were sorted in PCR plates, and DNA was amplified with primers specific for Vγ2-Jγ2 or Vγ6-Jγ1 rearrangements. (D) Presence (+) or absence (−) of specific amplification bands in 24 clones analyzed. (E) Junctional sequences of the Vγ6-Jγ1 amplifications present in 21 clones in D. GL denotes the germline sequences of the Vγ6 and Jγ1 ends as indicated. (F) LN cells from naive mice were stimulated with PMA/ionomycin, and total γδ T cells (top) or Vγ4+ cells (bottom) were gated and analyzed for intracellular IL-17 (middle) or IFN-γ (right) by FACS. Numbers indicate the percentage of cells inside the gates. One experiment representative of four is shown. The original FACS file was reanalyzed with FlowJo v10.3.

Vγ chain usage by γδ T17 cells in tumor bed and skin draining LNs of naive ...

in Correction: Contribution of IL-17–producing γδ T cells to the efficacy of anticancer chemotherapy > Journal of Experimental Medicine

Published: 12 February 2026

Figure S2. Vγ chain usage by γδ T17 cells in tumor bed and skin draining LNs of naive mice. (A) CD45, CD3, CD4, and TCR δ expression by IL-17A–producing cells from tumor beds of mice 8 d after chemotherapy. (B) Vγ usage in live CD45⁺ CD3⁺ TCR More about this image found in Vγ chain usage by γδ T17 cells in tumor bed and skin draining LNs of naive ...

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Untitled image

in Correction: B cell tolerance and antibody production to the celiac disease autoantigen transglutaminase 2 > Journal of Experimental Medicine

Published: 12 February 2026

More about this image found in Untitled image

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Generation of 14E06 KI mice. (A) Generation of the VDJH 14E06 KI mouse. Top: Targeting construct for the rearranged VDJH 14E06 and a FRT-flanked pkg-neo selection cassette. Middle: Mouse H chain locus with indication of the replaced D and J1-4 gene segments. Dashed lines indicate terminal points of homologous recombination. Bottom: Integrated transgene after flp mediated excision of the FRT-flanked neomycin selection gene. (B) Generation of the VJκ 14E06 KI mouse. Top: Targeting construct for the rearranged VJκ 14E06. Middle: Mouse κ L chain locus with indication of the replaced J1-5 gene segments. Bottom: integrated transgene after flp mediated excision of the FRT-flanked neomycin selection gene. (C) Detection of transgenic anti-TG2 BCR. Spleen cells from WT C57Bl/6 mice (obtained from Janvier Laboratoires), 14E06 L chain single KI and H chain single KI littermate control mice, and H and L chain double KI mice on C57Bl/6 background were stained using anti-B220 and an antibody specific for the H and L chain combination of 14E06 (anti-14E06) or mTG2 tetramers. Data are representative of two independent experiments.

Generation of 14E06 KI mice. (A) Generation of the VDJH 14E06 KI mouse. To...

in Correction: B cell tolerance and antibody production to the celiac disease autoantigen transglutaminase 2 > Journal of Experimental Medicine

Published: 12 February 2026

Figure 1. Generation of 14E06 KI mice. (A) Generation of the VDJH 14E06 KI mouse. Top: Targeting construct for the rearranged VDJH 14E06 and a FRT-flanked pkg-neo selection cassette. Middle: Mouse H chain locus with indication of the replaced D More about this image found in Generation of 14E06 KI mice. (A) Generation of the VDJH 14E06 KI mouse. To...

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Phenotype and regulatory mechanisms of DOT cells. DOT cells are in vitro–expanded γδ T cells that mostly (>70%) express a Vδ1+ TCR, which controls their activation, proliferation, and differentiation during the 2–3-wk protocol (Almeida et al., 2016). The cytokines IL-2 and IL-4 provide important signals for DOT cell proliferation, whereas IL-15 drives their cytotoxic effector phenotype. During in vitro expansion, strong TCR stimulation in the presence of IL-15 upregulates a series of NKRs that are critical for tumor cell targeting: NKp30 (binding to B7-H6 on tumor cells), DNAM-1 (binding to PVR and Nectin-2), and NKG2D (binding to MICA/B and ULBP1–6 ligands). Conversely, DOT cell activity is negatively regulated by TIGIT and PD-1, which are induced in the TME. The DOT cell protocol also upregulates chemokine receptors, like CXCR3 and CXCR4, that control their migration and infiltration into tumor lesions, and several molecules associated with tissue retention and residency, namely CD69 or CD103, alike tissue-resident memory T cells. Finally, DOT cells are very amenable to genetic engineering, and transduction with CARs specific for tumor-associated antigens (TAA) enhances their potency in vitro and in vivo.

Phenotype and regulatory mechanisms of DOT cells. DOT cells are in vitro–e...

in Follow the “DOTs”: Vδ1⁺ γδ T cells as effectors of cancer immunotherapy > Journal of Experimental Medicine

Published: 11 February 2026

Figure 1. Phenotype and regulatory mechanisms of DOT cells. DOT cells are in vitro–expanded γδ T cells that mostly (>70%) express a Vδ1⁺ TCR, which controls their activation, proliferation, and differentiation during the 2–3-wk protocol ( More about this image found in Phenotype and regulatory mechanisms of DOT cells. DOT cells are in vitro–e...

Journal Articles

Follow the “DOTs”: Vδ1⁺ γδ T cells as effectors of cancer immunotherapy

Bruno Silva-Santos, Sofia Mensurado, Rafael Blanco-Domínguez, Adrian C. Hayday

J Exp Med (2026) 223 (3): e20252289.

https://doi.org/10.1084/jem.20252289

Published: 11 February 2026

View article titled, Follow the “DOTs”: Vδ1+ γδ T cells as effectors of cancer immunotherapy

Journal Articles

Nasal germinal centers and IgA class-switch recombination depend on CCR6 and B cell receptor affinity

Jingjing Liu, Liat Stoler-Barak, Ziv Shulman

J Exp Med (2026) 223 (4): e20251901.

https://doi.org/10.1084/jem.20251901

Published: 10 February 2026

View article titled, Nasal germinal centers and IgA class-switch recombination depend on CCR6 and B cell receptor affinity

Journal Articles

Liver-X-receptor agonism enhances T cell priming and activation to promote anti-tumor immunity

Benjamin N. Ostendorf, Jonathan G. Goldstein, Shuang Liu, Foster C. Gonsalves, Jana Bilanovic, Mathias Yuan, Ji-Young Kim, Christopher Rouya, Masoud Tavazoie, Sohail F. Tavazoie

J Exp Med (2026) 223 (4): e20252290.

https://doi.org/10.1084/jem.20252290

Published: 10 February 2026

View article titled, Liver-X-receptor agonism enhances T cell priming and activation to promote anti-tumor immunity

Includes: Supplementary data

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B cells carrying low-affinity BCR are unable to seed GC in the NALT. (A) Schematic representation of the experimental setup shown in B–D. (B) AID-GFP mice were injected with Rosa26tdTomato/+ B1-8hi or B1-8lo B cells mixed with nonfluorescent CD4+ OT-II T cells followed by i.n. immunization with NP-OVA + MPLA. TPLSM images of NALT and MedLN 5 days following immunization are shown. n = 3 for each time point; two independent experiments. (C and D) WT mice were adaptively transferred with GFP+ B1-8hi or Rosa26tdTomato/+ B1-8lo B cells mixed with nonfluorescent CD4+ OT-II T cells. LNs were analyzed by flow cytometry 5 days after i.n. NP-OVA + MPLA immunization. n = 6; two independent experiments. Unpaired two-tailed Student’s t test; data represent mean ± SEM; *, P < 0.05; **, P < 0.01; ***, P < 0.001. (E) Experimental design for F. (F) Flow cytometry plots and frequency of B1-8hi or B1-8lo B cells 7 days after i.n. NP-OVA + MPLA boost. n = 6; two independent experiments. Unpaired two-tailed Student’s t test; data represent mean ± SEM; ***, P < 0.001.

B cells carrying low-affinity BCR are unable to seed GC in the NALT. (A) S...

in Nasal germinal centers and IgA class-switch recombination depend on CCR6 and B cell receptor affinity > Journal of Experimental Medicine

Published: 10 February 2026

Figure 1. B cells carrying low-affinity BCR are unable to seed GC in the NALT. (A) Schematic representation of the experimental setup shown in B–D. (B) AID-GFP mice were injected with Rosa26^tdTomato/+ B1-8^hi or B1-8^lo B cells mixed with More about this image found in B cells carrying low-affinity BCR are unable to seed GC in the NALT. (A) S...

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Low-affinity B cell clones are unable to seed GCs in the NALT independent of competition. (A) MD4 mice were adoptively transferred with GFP+ B1-8hi or Rosa26tdTomato/+ B1-8lo B cells. NALT and MedLN were removed and imaged by TPLSM on day 7 following i.n. NP-OVA + MPLA immunization. Scale bars, 200 µm. n = 4 for each time point; two independent experiments. (B–D) MD4 mice were injected with GFP+ B1-8hi or Rosa26tdTomato/+ B1-8lo B cells. NALT and MedLN were collected and analyzed by flow cytometry on day 3, 5, and 7 following i.n. NP-OVA + MPLA immunization. Representative plots for GC B cells on day 5 are shown (B). Flow cytometry quantification for GC B cell percentage of B1-8hi or B1-8lo B cells. Day 3, n = 5–6; day 5, n = 4–6; day 7, n = 5–7; six independent experiments. Unpaired two-tailed Student’s t test; data represent mean ± SEM; *, P < 0.05; **, P < 0.01; ***, P < 0.0001; ns, not significant (C and D). (E and F) MD4 mice were injected with Rosa26tdTomato/+ B1-8hi or B1-8lo B cells mixed with CD45.1+ OT-II T cells. LNs, BM, and spleen were collected and analyzed by flow cytometry on day 14 following i.n. NP-OVA + MPLA immunization. n = 5–6; two independent experiments. Unpaired two-tailed Student’s t test; data represent mean ± SEM; ns, not significant. Flow cytometry quantifications for total transferred cells (E) and GC B1-8hi or B1-8low B cells (F) are shown. (G and H) WT mice were injected with Rosa26tdTomato/+ B1-8hi or B1-8lo B cells. LNs were analyzed by flow cytometry 5 days after i.n. NP-Ficoll + MPLA immunization. n = 6; two independent experiments. Unpaired two-tailed Student’s t test; data represent mean ± SEM; **, P < 0.01; ns, not significant.

Low-affinity B cell clones are unable to seed GCs in the NALT independent o...

in Nasal germinal centers and IgA class-switch recombination depend on CCR6 and B cell receptor affinity > Journal of Experimental Medicine

Published: 10 February 2026

Figure 2. Low-affinity B cell clones are unable to seed GCs in the NALT independent of competition. (A) MD4 mice were adoptively transferred with GFP⁺ B1-8^hi or Rosa26^tdTomato/+ B1-8^lo B cells. NALT and MedLN were removed and imaged by TPLSM on More about this image found in Low-affinity B cell clones are unable to seed GCs in the NALT independent o...

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Formation of Tfh cells in the NALT depends on BCR affinity. (A–F) WT mice were injected with GFP+ B1-8hi or Rosa26tdTomato/+ B1-8lo B cells mixed with CD45.1+ OT-II T cells. Flow cytometry analysis of OT-II T cells was performed at day 5 following i.n. NP-OVA + MPLA immunization. n = 6; two independent experiments. Unpaired two-tailed Student’s t test; data represent mean ± SEM. *, P < 0.05; **, P < 0.01; ns, not significant. Flow cytometry plots and quantification of total OT-II T cells (A and B), activated CD44+ CD62L− OT-II T cells (C and D), CXCR5+ PD-1+ Tfh cells out of activated OT-II T cells (E and F) are shown. (G and H) Time course analysis of Tfh OT-II T cells formation in WT mice as in A. Day 1 n = 3; day 3, n = 3; day 5 n = 3; day 7 n = 2–3; one experiment. Unpaired two-tailed Student’s t test; data represent mean ± SEM. (I) Same experiment as in G using MD4 hosts. Day 3, n = 5–6; day 5, n = 8–9; day 7, n = 2–4; three independent experiments. Unpaired two-tailed Student’s t test; data represent mean ± SEM.

Formation of Tfh cells in the NALT depends on BCR affinity. (A–F) WT mice ...

in Nasal germinal centers and IgA class-switch recombination depend on CCR6 and B cell receptor affinity > Journal of Experimental Medicine

Published: 10 February 2026

Figure 3. Formation of Tfh cells in the NALT depends on BCR affinity. (A–F) WT mice were injected with GFP⁺ B1-8^hi or Rosa26^tdTomato/+ B1-8^lo B cells mixed with CD45.1⁺ OT-II T cells. Flow cytometry analysis of OT-II T cells was performed at day More about this image found in Formation of Tfh cells in the NALT depends on BCR affinity. (A–F) WT mice ...

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GC formation by high-affinity B cell clones depends on CCR6 expression. (A) WT mice were adoptively transferred with GFP+ B1-8hi B cells and CD45.1+ OT-II T cells. CCR6 expression on B1-8hi B cells was assessed by flow cytometry at the indicated time points after i.n. NP-OVA + MPLA immunization. Day 1, n = 3; day 3, n = 9; day 5, n = 9; day 7, n = 9; three independent experiments. Data represent mean ± SEM. (B) WT mice were adoptively transferred with GFP+ B1-8hi or Rosa26tdTomato/+ B1-8lo B cells, together with CD45.1+ OT-II T cells. The frequency of CCR6 expressing B1-8hi and B1-8lo B cells was analyzed by flow cytometry at the indicated time points. Day 3, n = 3–9; day 5, n = 3–9; day 7, n = 2–9; three independent experiments. Data represent mean ± SEM. (C) WT mice were adoptively transferred with GFP+ CCR6+/+ or CCR6−/− B1-8hi B cells, and Rosa26tdTomato/+ OT-II T cells. NALTs were imaged on days 3, 5, and 7 after i.n. NP-OVA + MPLA immunization, using TPLSM. Scale bars, 200 µm. For each time point, n = 2–4 mice; two independent experiments. (D–G) WT mice were adoptively transferred with GFP+ CCR6+/+ or CCR6−/− B1-8hi B cells and Rosa26tdTomato/+ OT-II T cells. Transferred cells (D), GC B cells (E), OT-II T cells (F), and OT-II Tfh T cells (G) subsets were quantified by flow cytometry on day 7 following i.n. NP-OVA + MPLA immunization. n = 5–11; three independent experiments. Unpaired two-tailed Student’s t test; data represent mean ± SEM; *, P < 0.05; **, P < 0.01; ****, P < 0.0001.

GC formation by high-affinity B cell clones depends on CCR6 expression. (A)...

in Nasal germinal centers and IgA class-switch recombination depend on CCR6 and B cell receptor affinity > Journal of Experimental Medicine

Published: 10 February 2026

Figure 4. GC formation by high-affinity B cell clones depends on CCR6 expression. (A) WT mice were adoptively transferred with GFP⁺ B1-8^hi B cells and CD45.1⁺ OT-II T cells. CCR6 expression on B1-8^hi B cells was assessed by flow cytometry at the More about this image found in GC formation by high-affinity B cell clones depends on CCR6 expression. (A)...

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IgA class switching in the NALT depends on CCR6-mediated B cell positioning in the SED. (A) CX3CR1-GFP mice were adoptively transferred with Rosa26tdTomato/+ B1-8hi B cells and CD45.1+ OT-II T cells. NALTs were imaged on day 5 after i.n. NP-OVA + MPLA immunization using TPLSM. Scale bars, 50–100 µm. n = 2; one experiment. (B) AicdaCre/+ Rosa26Stop-tdTomato/+ mice were adoptively transferred with GFP+ CCR6+/+ or CCR6−/− B1-8hi B cells and CD45.1+ OT-II T cells. NALTs were imaged on day 5 after i.n. NP-OVA + MPLA immunization using TPLSM. Scale bars, 100 µm. n = 3; one experiment. (C–F) WT mice were adoptively transferred with GFP+ CCR6+/+ or CCR6−/− B1-8hi B cells and OT-II T cells followed by NP-OVA + MPLA i.n. immunization. Transferred B1-8hi B cells (C) and IgA+ GC subsets (D) were quantified by flow cytometry on day 5; the frequency of IgA+ B cells was quantified out of the total transferred cells (E) or GC B cells (F) on day 7. Day 5, n = 6–7; day 7, n = 11; four independent experiments. Unpaired two-tailed Student’s t test; Data represent mean ± SEM; ***, P < 0.001; ****, P < 0.0001; ns, not significant.

IgA class switching in the NALT depends on CCR6-mediated B cell positioning...

in Nasal germinal centers and IgA class-switch recombination depend on CCR6 and B cell receptor affinity > Journal of Experimental Medicine

Published: 10 February 2026

Figure 5. IgA class switching in the NALT depends on CCR6-mediated B cell positioning in the SED. (A) CX₃CR1-GFP mice were adoptively transferred with Rosa26^tdTomato/+ B1-8^hi B cells and CD45.1⁺ OT-II T cells. NALTs were imaged on day 5 after More about this image found in IgA class switching in the NALT depends on CCR6-mediated B cell positioning...

Images

CCR6 is required for bacteria-driven IgA GC B cell formation in the NALT. (A) Quantification by flow cytometry of B cell isotypes in NALTs from SPF or GF mice under homeostasis. IgA+, IgG2b+, and IgG1+ populations were gated from Fas+CD38−B220+ GC B cells. n = 8–10; two independent experiments. Unpaired two-tailed Student’s t test; data represent mean ± SEM; **, P < 0.01. (B) Flow cytometry analysis of GC B cells in NALT from CCR6+/+ or CCR6−/− SPF mice. n = 6–10; three independent experiments. Unpaired two-tailed Student’s t test; data represent mean ± SEM; *, P < 0.05. (C) Experimental design of mixed BM chimeras generated with CCR6+/+ and CCR6−/− donors. (D–G) Flow cytometry analysis of B cell subsets in NALTs from BM chimeras. CCR6+/+ and CCR6−/− B cells were gated from B220+ B cells (D); GC (Fas+CD38−) B cell populations were gated from CCR6+/+ or CCR6−/− B220+ cells in D (E); IgA+ and IgG2b+ populations were gated from CCR6+/+ or CCR6−/− B220+ cells (F), or from CCR6+/+ or CCR6−/− GC B cells (G). n = 9; two independent experiments. Paired two-tailed Student’s t test; data represent mean ± SEM; *, P < 0.05.

CCR6 is required for bacteria-driven IgA GC B cell formation in the NALT. (...

in Nasal germinal centers and IgA class-switch recombination depend on CCR6 and B cell receptor affinity > Journal of Experimental Medicine

Published: 10 February 2026

Figure 6. CCR6 is required for bacteria-driven IgA GC B cell formation in the NALT. (A) Quantification by flow cytometry of B cell isotypes in NALTs from SPF or GF mice under homeostasis. IgA⁺, IgG2b⁺, and IgG1⁺ populations were gated from Fas⁺ More about this image found in CCR6 is required for bacteria-driven IgA GC B cell formation in the NALT. (...

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LXR agonism exhibits treatment efficacy in breast and colon cancer models with low G-MDSC infiltration. (a) Abundance of Ly6G+ G-MDSCs across different syngeneic tumor models (n = 7, 7, 6, 8, and 6 for LLC, B16F10, E0771, E0771-DR, and CT26, respectively). (b) Representative flow cytometry plots representing the abundance of Ly6G+ and Ly6C+ MDSCs in the LLC and E0771 tumor models. (c) Abundance of Ly6G+ G-MDSCs in E0771-DR tumors upon LXR-agonistic treatment with RGX-104 (n ≥ 8 per group, two-sided t test). (d) Growth of orthotopic E0771-DR tumors and survival upon LXR-agonistic treatment (n ≥ 7 per group, two-tailed t test for tumor growth and log-rank test for survival, representative of three independent experiments). (e) Metastatic progression of E0771-LM1-DR tumors as quantified by bioluminescence imaging (n = 7 per group, two-tailed Mann–Whitney test; images correspond to representative mice on day 20 after injection). (f) Abundance of G-MDSCs in CT26 tumors upon RGX-104 treatment (n = 8 per group, two-tailed t test). (g) Growth of CT26 tumors upon RGX-104 treatment (n ≥ 6 per group; two-tailed t test). n.s., not significant. All experiments representative of two independent experiments unless indicated otherwise. *P < 0.05 and **P < 0.01.

LXR agonism exhibits treatment efficacy in breast and colon cancer models w...

in Liver-X-receptor agonism enhances T cell priming and activation to promote anti-tumor immunity > Journal of Experimental Medicine

Published: 10 February 2026

Figure 1. LXR agonism exhibits treatment efficacy in breast and colon cancer models with low G-MDSC infiltration. (a) Abundance of Ly6G⁺ G-MDSCs across different syngeneic tumor models (n = 7, 7, 6, 8, and 6 for LLC, B16F10, E0771, E0771-DR, and More about this image found in LXR agonism exhibits treatment efficacy in breast and colon cancer models w...

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LXR agonism promotes adaptive anti-tumor immunity in breast and colon cancer models. (a and b) Tumor growth and survival of naive mice or mice that had cleared E0771-DR tumors under LXR-agonism upon contralateral primary tumor (a) or metastatic (b) rechallenge with E0771 cells (n ≥ 8 per group, log-rank test, and data pooled from two independent experiments). (c) Intratumoral CD8+ T cell infiltration in E0771-DR tumors (n = 7; two-tailed t test). Images show representative sections (scale bar = 100 μm). All P values are based on two-tailed t tests. (d–f) Expression of granzyme B by CD8+ cytotoxic T cells infiltrating E0771-DR (d) and CT26 tumors (f) (n = 8 per group, two-tailed t test, representative of three and two independent experiments, respectively). Flow cytometry plots in e are representative for results in d. (g) Growth of E0771-DR mammary fat pad tumors in C57BL/6J wild-type versus Rag−/− mice (n ≥ 4 per group; two-tailed t test; representative of two independent experiments). (h) Growth of E0771-DR mammary fat pad tumors upon depletion of CD8+ cells (n ≥ 6 per group, two-tailed t test; representative of two independent experiments). *P < 0.05 and ****P < 0.0001.

LXR agonism promotes adaptive anti-tumor immunity in breast and colon cance...

in Liver-X-receptor agonism enhances T cell priming and activation to promote anti-tumor immunity > Journal of Experimental Medicine

Published: 10 February 2026

Figure 2. LXR agonism promotes adaptive anti-tumor immunity in breast and colon cancer models. (a and b) Tumor growth and survival of naive mice or mice that had cleared E0771-DR tumors under LXR-agonism upon contralateral primary tumor (a) or More about this image found in LXR agonism promotes adaptive anti-tumor immunity in breast and colon cance...

Images

LXR agonism enhances immune activation in tumor DLNs. (a–c) Phenotype of DLN-resident CD4+ and CD8+ T cells in E0771-cOC (a) or CT26-DR (c) tumor-bearing mice treated with RGX-104 (n = 8 and 7 per group, respectively, two-tailed t tests; representative of two independent experiments). Flow cytometry plots in b show representative samples gated for CD8+ T cells from a. (d–f) Proportion of all T cell subsets (d) and only cytotoxic T cells (e) out of all T cells in E0771-DR tumor DLNs as assessed by scRNAseq. (f) Comparison of the expression of select canonical effector genes in cytotoxic T cells in control versus RGX-104–treated mice (P values according to Mann–Whitney tests). (g–i) Activation status of APCs in the LNs draining E0771-cOC (g) and CT26 (h) tumors (n = 15 [g] and 7 [h] per group; two-tailed t tests, each representative of two independent experiments). (i) Representative plots from h showing expression of MHCII, CD40, and CD86 in CD103+ DCs. MHCII, MHC class II. *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001.

LXR agonism enhances immune activation in tumor DLNs. (a–c) Phenotype of D...

in Liver-X-receptor agonism enhances T cell priming and activation to promote anti-tumor immunity > Journal of Experimental Medicine

Published: 10 February 2026

Figure 3. LXR agonism enhances immune activation in tumor DLNs. (a–c) Phenotype of DLN-resident CD4⁺ and CD8⁺ T cells in E0771-cOC (a) or CT26-DR (c) tumor-bearing mice treated with RGX-104 (n = 8 and 7 per group, respectively, two-tailed t More about this image found in LXR agonism enhances immune activation in tumor DLNs. (a–c) Phenotype of D...

Images

LXR agonistic therapy critically depends on CD11c+DCs and host Lxr but not Apoe expression. (a) Schematic of strategy for in vivo depletion of APC subsets. (b) Growth of orthotopic E0771-DR tumors in the presence or absence of CD11c+ cells as outlined in a (n = 14–16 per group, two-tailed t test, data pooled from two independent experiments). (c) Abundance of APC subsets in tumor DLNs and tumors of E0771-DR tumor bearing–mice transplanted with Itgax-DTR bone marrow and treated with PBS or DT (two-tailed t tests). Images show representative flow cytometry plots (n = 6–8 per group, two-tailed t tests). (d) Growth of orthotopic E0771-DR tumors in the presence or absence of LyzM+Csf1r+ cells (n = 7–9 per group, two tailed t test, representative of two independent experiments). (e) Abundance of APC subsets in DLNs or tumors of E0771-DR tumor bearing–mice transplanted with MM-DTR bone marrow and treated with PBS or DT (two-tailed t tests). Images show representative flow cytometry plots (n = 4 per group, two-tailed t tests). (f) Fraction of Ly6C+ monocytes out of CD45+ cells in peripheral blood of MM-DTR mice treated with either PBS or DT (n = 4 per group, P value according to one-sided T test). (g) Growth of E0771-DR in C57BL/6J wild-type versus Apoe-KO mice (n ≥ 11 mice per group, respectively; data pooled from two independent experiments). (h) Growth of E0771-DR tumors in APOE2-knock-in mice (n = ≥15 mice per group; two-tailed t test). (i) Growth of E0771-DR tumors in C57BL6/J wild-type versus Lxr-DKO mice (n ≥ 10 mice per group, representative of two independent experiments; two-tailed t test). MHCII, MHC class II. *P < 0.05, **P < 0.01, and ***P < 0.001.

LXR agonistic therapy critically depends on CD11c ⁺ DCs and ho...

in Liver-X-receptor agonism enhances T cell priming and activation to promote anti-tumor immunity > Journal of Experimental Medicine

Published: 10 February 2026

Figure 4. LXR agonistic therapy critically depends on CD11c ⁺ DCs and host Lxr but not Apoe expression. (a) Schematic of strategy for in vivo depletion of APC subsets. (b) Growth of orthotopic E0771-DR tumors in the presence or absence of More about this image found in LXR agonistic therapy critically depends on CD11c ⁺ DCs and ho...

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