ArticleCancer research2012
Antigen-specific CD4(+) T cells regulate function of myeloid-derived suppressor cells in cancer via retrograde MHC class II signaling.
Article in Cancer research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
54 citing papers in PubMed, 102 citations in OpenAlex.
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- Characterization of Dendritic Cells and Myeloid-Derived Suppressor Cells Expressing Major Histocompatibility Complex Class II in Secondary Lymphoid Organs in Systemic Lupus Erythematosus-Prone Mice.International journal of molecular sciences · 2024Article
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- Cancer CD39 drives metabolic adaption and mal-differentiation of CD4Cell death & disease · 2023Article
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- Immunophenotyping of Circulating and Intratumoral Myeloid and T Cells in Glioblastoma Patients.Cancers · 2022Article
- Polyamines in cancer: integrating organismal metabolism and antitumour immunity.Nature reviews. Cancer · 2022Review
- Myeloid-derived suppressor cells in cancer.iLIVER · 2022Review
- Development of Bispecific Antibody for Cancer Immunotherapy: Focus on T Cell Engaging Antibody.Immune network · 2022Review
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- Myeloid Cell-Derived Oxidized Lipids and Regulation of the Tumor Microenvironment.Cancer research · 2022Review
- Sustained Drug Release From Liposomes for the Remodeling of Systemic Immune Homeostasis and the Tumor Microenvironment.Frontiers in immunology · 2022Article
- Myeloid-derived suppressor cells and vaccination against pathogens.Frontiers in cellular and infection microbiology · 2022Review
- A nomogram-based immunoprofile predicts clinical outcomes for stage II and III human colorectal cancer.Molecular and clinical oncology · 2021Article
- Myeloid cell subsets that express latency-associated peptide promote cancer growth by modulating T cells.iScience · 2021Article
- Homocitrullination of lysine residues mediated by myeloid-derived suppressor cells in the tumor environment is a target for cancer immunotherapy.Journal for immunotherapy of cancer · 2021Article
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- Donor myeloid derived suppressor cells (MDSCs) prolong allogeneic cardiac graft survival through programming of recipient myeloid cells in vivo.Scientific reports · 2020Article
- Renal cancer-derived exosomes induce tumor immune tolerance by MDSCs-mediated antigen-specific immunosuppression.Cell communication and signaling : CCS · 2020Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Myeloid-derived suppressor cells (MDSC) play a major role in cancer-related immune suppression, yet the nature of this suppression remains controversial. In this study, we evaluated the ability of MDSCs to elicit CD4(+) T-cell tolerance in different mouse tumor models. In contrast to CD8(+) T-cell tolerance, which could be induced by MDSCs in all the tumor models tested, CD4(+) T-cell tolerance could be elicited in only one of the models (MC38) in which a substantial level of MHC class II was expressed on MDSCs compared with control myeloid cells. Mechanistic investigations revealed that MDSCs deficient in MHC class II could induce tolerance to CD8(+) T cells but not to CD4(+) T cells. Unexpectedly, antigen-specific CD4(+) T cells (but not CD8(+) T cells) could dramatically enhance the immune suppressive activity of MDSCs by converting them into powerful nonspecific suppressor cells. This striking effect was mediated by direct cell-cell contact through cross-linking of MHC class II on MDSCs. We also implicated an Ets-1 transcription factor-regulated increase in expression of Cox-2 and prostaglandin E2 in MDSCs in mediating this effect. Together, our findings suggest that activated CD4(+) T cells that are antigen specific may enhance the immune suppressive activity of MDSCs, a mechanism that might serve normally as a negative feedback loop to control immune responses that becomes dysregulated in cancer.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.