Zoe C. Schmiechen
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Research Subjects
Zoe C. Schmiechen has a total of 72 co-authors. Here are the top co-authors by number of shared publications:
- Ingunn M. Stromnes
Department of Microbiology and Immunology, University of Minnesota, Minneapolis, USA
16 shared publications - Adam L. Burrack
Department of Microbiology and Immunology, University of Minnesota Medical School, Minneapolis, MN, USA
15 shared publications Ebony A. Miller
Department of Microbiology and Immunology, University of Minnesota Medical School, Minneapolis, MN, USA
14 shared publications- Eduardo Cruz-Hinojoza
Department of Microbiology and Immunology, University of Minnesota Medical School, Minneapolis, MN, USA
14 shared publications - Alexander K. Tsai
Division of Hematology, Oncology and Transplantation, Department of Medicine, University of Minnesota, Minneapolis, MN 55455, USA; Masonic Cancer Center, University of Minnesota, Minneapolis, MN 55455, USA; Center for Immunology, University of Minnesota, Minneapolis, MN 55455, USA
13 shared publications - Audrey L. Hilk
Department of Microbiology and Immunology, University of Minnesota Medical School, Minneapolis, MN, USA
13 shared publications
Latest Publications
- Open Access
- 8 August 2026
- Published by Elsevier in Cytotherapy
- Vol. 28 (12)
Hypoxia during GPC2-CAR T-cell manufacturing compromises cell expansion and cytotoxic capacity
- 8 August 2026
- Published by Elsevier in Cytotherapy
- Vol. 28 (12)
Open AccessHypoxia during GPC2-CAR T-cell manufacturing compromises cell expansion and cytotoxic capacity
- Open Access
Tumor-specific CD4 T cells cooperate with myeloid cells to remodel the pancreatic tumor microenvironment and enable effective immunotherapy
We interrogate antigen-specific CD4 T cells during immunotherapy in pancreatic ductal adenocarcinoma. Vaccination with MHC-II-restricted tumor epitopes impart superior protection compared to an immunodominant MHC-I epitope, prompting development of MHC-II affinity-enhanced tetramers to track tumor-specific CD4 T cells. As tumors progress, tumor-specific CD4 T cells decline, and remaining cells acquire features of regulation. Agonistic anti-CD40 increases Th1 cell clonal expansion and transiently decreases Tregs. Anti-PD-L1 promotes Tfh clonal expansion in draining lymph nodes and tumor while preventing Treg rebound after anti-CD40. Treatment with anti-CD40 promotes intratumoral Stat1 + macrophages, tertiary lymphoid structures (TLS), and immune triads. MHC-II on myeloid cells but not B cells is required for immunotherapy-induced TLS formation and antitumor effects. IL-15 complex enhances immunotherapy-induced Th1 effectors without promoting Tregs. Human immunotherapy transcriptomics shows conserved Th1 programming and Treg destabilization as a feature of response. Thus, tumor-specific CD4 T cells are central mediators of effective immunotherapy in solid tumors.
Open AccessTumor-specific CD4 T cells cooperate with myeloid cells to remodel the pancreatic tumor microenvironment and enable effective immunotherapy
We interrogate antigen-specific CD4 T cells during immunotherapy in pancreatic ductal adenocarcinoma. Vaccination with MHC-II-restricted tumor epitopes impart superior protection compared to an immunodominant MHC-I epitope, prompting development of MHC-II affinity-enhanced tetramers to track tumor-specific CD4 T cells. As tumors progress, tumor-specific CD4 T cells decline, and remaining cells acquire features of regulation. Agonistic anti-CD40 increases Th1 cell clonal expansion and transiently decreases Tregs. Anti-PD-L1 promotes Tfh clonal expansion in draining lymph nodes and tumor while preventing Treg rebound after anti-CD40. Treatment with anti-CD40 promotes intratumoral Stat1 + macrophages, tertiary lymphoid structures (TLS), and immune triads. MHC-II on myeloid cells but not B cells is required for immunotherapy-induced TLS formation and antitumor effects. IL-15 complex enhances immunotherapy-induced Th1 effectors without promoting Tregs. Human immunotherapy transcriptomics shows conserved Th1 programming and Treg destabilization as a feature of response. Thus, tumor-specific CD4 T cells are central mediators of effective immunotherapy in solid tumors.
- 26 June 2026
- Published by American Association for the Advancement of Science (AAAS) in Science Immunology
- Vol. 11 (120) , eadz4302
T reg cells promote immunotherapy-induced immune evasion by restraining CD4 T cell control of MHC-I–deficient metastatic pancreatic cancer
Mechanisms driving immunotherapy resistance in pancreatic cancer are poorly defined. We demonstrate that programmed death-ligand 1 immune checkpoint blockade promoted immune evasion by epigenetic Tap1 ( transporter associated with antigen processing 1 ) silencing, increasing selection of metastatic tumor variants with defective interferon-γ (IFN-γ)–inducible class I major histocompatibility complex (MHC-I) expression. Unleashing CD4 conventional T cells by regulatory T cell (T reg cell) depletion, transfer of tumor-reactive CD4 T cells, or anti–CTLA-4 prevented metastasis. Tumor-specific CD4 T cells adopted a TCF-1 + SLAMF6 + progenitor state in lymph nodes and differentiated in tumors. Anti–CTLA-4 increased intratumoral accumulation of CD4 T cells with stemness and tissue residency features, reduced metastasis, and induced gene signatures correlated with improved patient outcomes. MHC-I restoration with anti–CTLA-4 prolonged survival in murine models. In patient tumors, T reg cells and CD4 T cells colocalized, and abundance correlated with survival. These findings identify targetable mechanisms of immune evasion and metastasis in immunotherapy-resistant cancer.
- 26 June 2026
- Published by American Association for the Advancement of Science (AAAS) in Science Immunology
- Vol. 11 (120) , eadz4302
T reg cells promote immunotherapy-induced immune evasion by restraining CD4 T cell control of MHC-I–deficient metastatic pancreatic cancer
Mechanisms driving immunotherapy resistance in pancreatic cancer are poorly defined. We demonstrate that programmed death-ligand 1 immune checkpoint blockade promoted immune evasion by epigenetic Tap1 ( transporter associated with antigen processing 1 ) silencing, increasing selection of metastatic tumor variants with defective interferon-γ (IFN-γ)–inducible class I major histocompatibility complex (MHC-I) expression. Unleashing CD4 conventional T cells by regulatory T cell (T reg cell) depletion, transfer of tumor-reactive CD4 T cells, or anti–CTLA-4 prevented metastasis. Tumor-specific CD4 T cells adopted a TCF-1 + SLAMF6 + progenitor state in lymph nodes and differentiated in tumors. Anti–CTLA-4 increased intratumoral accumulation of CD4 T cells with stemness and tissue residency features, reduced metastasis, and induced gene signatures correlated with improved patient outcomes. MHC-I restoration with anti–CTLA-4 prolonged survival in murine models. In patient tumors, T reg cells and CD4 T cells colocalized, and abundance correlated with survival. These findings identify targetable mechanisms of immune evasion and metastasis in immunotherapy-resistant cancer.
- Open Access
- 4 June 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 5 from IL-15 Complex Enhances Agonistic Anti-CD40 + Anti-PDL1 by Correcting the T-bet to Tox Ratio in CD8+ T cells Infiltrating Pancreatic Ductal Adenocarcinoma
Antigen specificity and functionality of predominant TCRs from tumors from immunotherapy treated mice.
- 4 June 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 5 from IL-15 Complex Enhances Agonistic Anti-CD40 + Anti-PDL1 by Correcting the T-bet to Tox Ratio in CD8+ T cells Infiltrating Pancreatic Ductal Adenocarcinoma
Antigen specificity and functionality of predominant TCRs from tumors from immunotherapy treated mice.
- Open Access
- 4 June 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 1 from IL-15 Complex Enhances Agonistic Anti-CD40 + Anti-PDL1 by Correcting the T-bet to Tox Ratio in CD8+ T cells Infiltrating Pancreatic Ductal Adenocarcinoma
Single cell transcriptional atlas following anti-PDL1 or agonistic anti-CD40
- 4 June 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 1 from IL-15 Complex Enhances Agonistic Anti-CD40 + Anti-PDL1 by Correcting the T-bet to Tox Ratio in CD8+ T cells Infiltrating Pancreatic Ductal Adenocarcinoma
Single cell transcriptional atlas following anti-PDL1 or agonistic anti-CD40
- Open Access
- 4 June 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 6 from IL-15 Complex Enhances Agonistic Anti-CD40 + Anti-PDL1 by Correcting the T-bet to Tox Ratio in CD8+ T cells Infiltrating Pancreatic Ductal Adenocarcinoma
CD4 T cells and tumor antigen are required for anti-CD40 driven TSTEM accumulation in PDA
- 4 June 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 6 from IL-15 Complex Enhances Agonistic Anti-CD40 + Anti-PDL1 by Correcting the T-bet to Tox Ratio in CD8+ T cells Infiltrating Pancreatic Ductal Adenocarcinoma
CD4 T cells and tumor antigen are required for anti-CD40 driven TSTEM accumulation in PDA
- Open Access
- 4 June 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 4 from IL-15 Complex Enhances Agonistic Anti-CD40 + Anti-PDL1 by Correcting the T-bet to Tox Ratio in CD8+ T cells Infiltrating Pancreatic Ductal Adenocarcinoma
Comparison of human and murine tumor-infiltrating CD8 T cells.
- 4 June 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 4 from IL-15 Complex Enhances Agonistic Anti-CD40 + Anti-PDL1 by Correcting the T-bet to Tox Ratio in CD8+ T cells Infiltrating Pancreatic Ductal Adenocarcinoma
Comparison of human and murine tumor-infiltrating CD8 T cells.
- Open Access
- 4 June 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 9 from IL-15 Complex Enhances Agonistic Anti-CD40 + Anti-PDL1 by Correcting the T-bet to Tox Ratio in CD8+ T cells Infiltrating Pancreatic Ductal Adenocarcinoma
IL15C synergizes with immunotherapy to target poorly immunogenic KPC2 tumors
- 4 June 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 9 from IL-15 Complex Enhances Agonistic Anti-CD40 + Anti-PDL1 by Correcting the T-bet to Tox Ratio in CD8+ T cells Infiltrating Pancreatic Ductal Adenocarcinoma
IL15C synergizes with immunotherapy to target poorly immunogenic KPC2 tumors
- Open Access
- 4 June 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Figure 3 from IL-15 Complex Enhances Agonistic Anti-CD40 + Anti-PDL1 by Correcting the T-bet to Tox Ratio in CD8+ T cells Infiltrating Pancreatic Ductal Adenocarcinoma
CD8 T cell differentiation in PDA.
- 4 June 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figure 3 from IL-15 Complex Enhances Agonistic Anti-CD40 + Anti-PDL1 by Correcting the T-bet to Tox Ratio in CD8+ T cells Infiltrating Pancreatic Ductal Adenocarcinoma
CD8 T cell differentiation in PDA.