Cancer Immune Evasion Through Loss of MHC Class I Antigen Presentation

Dhatchinamoorthy, Karthik; Colbert, Jeff D.; Rock, Kenneth L.

doi:10.3389/fimmu.2021.636568

Cited by 1,077Cancer Immunotherapy and BiomarkersImmunotherapy and Immune ResponsesT-cell and B-cell Immunology

Cancer Immune Evasion Through Loss of MHC Class I Antigen Presentation

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Dhatchinamoorthy, Karthik, Colbert, Jeff D., Rock, Kenneth L.·2021·Frontiers in Immunology

DOI 10.3389/fimmu.2021.636568PMC PMC7986854

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Abstract

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 its MHC-free nature that makes the host immune system recognize them as self-components.
“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]
In “Recognition and Control of MHC I Low Cancers by NK Cells” (page unavailable), the paper says NK cells ignore normal MHC I-sufficient cells but can detect abnormal cells with low MHC I; it does not say that MHC absence makes the immune system recognize something as self. The paper does not discuss natural scaffolds or their biocompatibility, so the contrary evidence concerns the claim’s proposed immune-recognition mechanism, not scaffold outcomes. (LLM, conf=0.76)
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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.
“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]
The Introduction and the section on mutation or deletion of structural genes explain that cancers can evade CD8 T cells through loss of MHC I antigen presentation, including loss of MHC I genes. Figure 4 includes GBM among cancers assessed for MHC I loss, but the text of our copy does not establish that loss of a required HLA allele or presentation-pathway defects are less common in GBM than in other tumour types; its frequency comparison concerns MHC I expression more generally. No page numbers are available in our copy. (LLM, conf=0.86)
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Lu, 2000, Decreased HLA-A expression in prostate cancer is associated with normal allele dosage in the majority of cases, J Pathol, 190, 169, 10.1002/(SICI)1096-9896(200002)190:2169::AID-PATH517>3.0.CO;2-# · DOI

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Authors: Dhatchinamoorthy, K., Colbert, J. D., & Rock, K. L.
Affiliations: University of Massachusetts Chan Medical School (US)
Corresponding author: Rock, Kenneth L.
ORCID: Dhatchinamoorthy, Karthik
Colbert, Jeff D.
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)
DOI: 10.3389/fimmu.2021.636568
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: cc-by
creativecommons.org/licenses/by/4.0/ (vor)
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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Cancer Immune Evasion Through Loss of MHC Class I Antigen Presentation

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