The DOI matches its Crossref record; 423 of the 429 references it cites were found in a registry or an index.
Cancer Immune Evasion Through Loss of MHC Class I Antigen Presentation
Open accessAbstract
Major histocompatibility class I (MHC I) molecules bind peptides derived from a cell's expressed genes and then transport and display this antigenic information on the cell surface. This allows CD8 T cells to identify pathological cells that are synthesizing abnormal proteins, such as cancers that are expressing mutated proteins. In order for many cancers to arise and progress, they need to evolve mechanisms to avoid elimination by CD8 T cells. MHC I molecules are not essential for cell survival and therefore one mechanism by which cancers can evade immune control is by losing MHC I antigen presentation machinery (APM). Not only will this impair the ability of natural immune responses to control cancers, but also frustrate immunotherapies that work by re-invigorating anti-tumor CD8 T cells, such as checkpoint blockade. Here we review the evidence that loss of MHC I antigen presentation is a frequent occurrence in many cancers. We discuss new insights into some common underlying mechanisms through which some cancers inactivate the MHC I pathway and consider some possible strategies to overcome this limitation in ways that could restore immune control of tumors and improve immunotherapy.
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“Desirable biocompatibility of natural scaffolds is primarily ascribed to the inter- and intra-species conservation of ECM [27] and its MHC-free nature that makes the host immune system recognize them as self-components [28].”
From Immunogenicity of decellularized extracellular matrix scaffolds: a bottleneck in tissue engineering and regenerative medicine (2023) · cites this paper as [28]
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“However, immune evasion can also occur by loss of the required HLA allele or defects in the HLA presentation pathway, although this is less common in GBM than other tumour types [40].”
From Preclinical development of an mRNA-based multiepitope immunotherapeutic for glioblastoma (2025) · cites this paper as [40]
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6 of the 429 references couldn’t be matched to a known paper.
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“Compared with CD8 T cells, NK cells serve as alternative sources of cytotoxic activities and combat tumor cells with low mutation load and aberrant expression of major histocompatibility complex (MHC) class I.(22,23) Although the dysfunctional state of CD8 T cells is well-characterized with reduced cytotoxicity”
Background
Metadata
- Authors
- Dhatchinamoorthy, K., Colbert, J. D., & Rock, K. L.
- Affiliations
- University of Massachusetts Chan Medical School (US)
- Corresponding author
- Rock, Kenneth L.
- Venue
- Frontiers in Immunology
- Publisher
- Frontiers Media SA
- Published
- 2021-03-09
- Volume
- 12
- Pages
- 636568-636568
- ISSN
- 1664-3224 (ISSN-L)
- PMC
- PMC7986854
- OpenAlex
- W3134746059
- Cited by
- 1,077
- References
- 429
- Citations by year
- 2026: 209 · 2025: 244 · 2024: 251 · 2023: 202 · 2022: 138 · 2021: 33
- FWCI
- 19.72
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Immunology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- eScholarship@UMassChan (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Cancer Institute (R01CA247624)
- National Institute of Allergy and Infectious Diseases (R01AI145932)
- Topics
- Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
- Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- tumor immune evasion, MHC class I antigen presentation, MHC class I loss, CD8+ T cells, cancer immunotherapy, immune checkpoint blockade, tumor antigens
- MeSH terms
- Animals, Humans, Killer Cells, Natural, Mutation, Neoplasms, Transcription, Genetic, Histocompatibility Antigens Class I, Signal Transduction, Gene Expression Regulation, Neoplastic, Lymphocytes, Tumor-Infiltrating, Gene Deletion, Antigen Presentation, Tumor Escape, Tumor Microenvironment
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