ArticleJournal of immunology (Baltimore, Md. : 1950)2012
Cellular and molecular requirements for rejection of B16 melanoma in the setting of regulatory T cell depletion and homeostatic proliferation.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 45 citations in OpenAlex.
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- Depletion of conventional CD4Journal for immunotherapy of cancer · 2024Article
- Batf3Cell reports · 2024Article
- Microbial ligand-independent regulation of lymphopoiesis by NOD1.Nature immunology · 2023Article
- Engineered skin bacteria induce antitumor T cell responses against melanoma.Science (New York, N.Y.) · 2023Article
- Interleukin-17 signaling influences CD8Oncoimmunology · 2023Article
- Dendritic cells can prime anti-tumor CD8Immunity · 2022Article
- Anti-Gr-1 Antibody Provides Short-Term Depletion of MDSC in Lymphodepleted Mice with Active-Specific Melanoma Therapy.Vaccines · 2022Article
- Identification of Highly Cross-Reactive Mimotopes for a Public T Cell Response in Murine Melanoma.Frontiers in immunology · 2022Article
- A diversity outbred F1 mouse model identifies host-intrinsic genetic regulators of response to immune checkpoint inhibitors.Oncoimmunology · 2022Article
- STING Sensing of Murine Cytomegalovirus Alters the Tumor Microenvironment to Promote Antitumor Immunity.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Tumor heterogeneity and clonal cooperation influence the immune selection of IFN-γ-signaling mutant cancer cells.Nature communications · 2020Article
- A tumor-targeted immune checkpoint blocker.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Requirement of Mitochondrial Transcription Factor A in Tissue-Resident Regulatory T Cell Maintenance and Function.Cell reports · 2019Article
- Adenovirus Coding for Interleukin-2 and Tumor Necrosis Factor Alpha Replaces Lymphodepleting Chemotherapy in Adoptive T Cell Therapy.Molecular therapy : the journal of the American Society of Gene Therapy · 2018Article
- Targeting of CD122 enhances antitumor immunity by altering the tumor immune environment.Oncotarget · 2017Article
- Heterodimeric IL15 Treatment Enhances Tumor Infiltration, Persistence, and Effector Functions of Adoptively Transferred Tumor-specific T Cells in the Absence of Lymphodepletion.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017Article
- The EGR2 targets LAG-3 and 4-1BB describe and regulate dysfunctional antigen-specific CD8+ T cells in the tumor microenvironment.The Journal of experimental medicine · 2017Article
- AIMp1 Potentiates TFrontiers in immunology · 2017Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
We have recently demonstrated that adoptive transfer of regulatory T cell-depleted polyclonal T cells into lymphopenic mice leads to rejection of B16 melanoma, which generated an opportunity to study host requirements for tumor rejection when it effectively occurred. CD8(+) T cell priming and tumor rejection required tumor Ag cross-presentation, as evidenced by tumor outgrowth in Kb(-/-) bone marrow chimeric or B71/2(-/-) mice. CD4(+) T cells were additionally required for optimal tumor control, although not through classical CD4 "help," as the frequency of primed CD8(+) T cells was similar in the absence of CD4(+) T cells, and tumor rejection did not depend upon CD40-CD40L interactions or on IL-2 production by CD4(+) T cells. Rather, CD4(+) T cells appeared to act at the effector phase of tumor rejection and responded to B16-derived Ags in vitro. At the effector phase, IFN-γ production by transferred T cells, but not host cells, was necessary. IFN-γ acted either on host or tumor cells and was associated with reduced tumor vascularity. Finally, tumor rejection occurred after transfer of TNF-α, perforin, or FasL-deficient T cells. However, perforin/FasL double-knockout T cells failed to reject, arguing that the killing of B16 melanoma cells could occur either via the cytotoxic granule or Fas pathways. Collectively, these results support a model in which host tumor Ag cross-presentation primes adoptively transferred T cells, which remain functional in the setting of homeostatic proliferation and regulatory T cell depletion, and which promote tumor rejection via IFN-γ and lysis via cytotoxic granules and/or FasL.
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