Learning from the nexus of autoimmunity and cancer
Open accessAbstract
The immune system plays critical roles in both autoimmunity and cancer, diseases at opposite ends of the immune spectrum. Autoimmunity arises from loss of T cell tolerance against self, while in cancer, poor immunity against transformed self fails to control tumor growth. Blockade of pathways that preserve self-tolerance is being leveraged to unleash immunity against many tumors; however, widespread success is hindered by the autoimmune-like toxicities that arise in treated patients. Knowledge gained from the treatment of autoimmunity can be leveraged to treat these toxicities in patients. Further, the understanding of how T cell dysfunction arises in cancer can be leveraged to induce a similar state in autoreactive T cells. Here, we review what is known about the T cell response in autoimmunity and cancer and highlight ways in which we can learn from the nexus of these two diseases to improve the application, efficacy, and management of immunotherapies.
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Inhibitory receptor deficiencies or checkpoint therapies can cause or exacerbate AIDs.
“Inhibitory receptor deficiencies or checkpoint therapies can cause or exacerbate AIDs, 37,61”
From Autoantigen-specific CD4+ T cells acquire an exhausted phenotype and persist in human antigen-specific autoimmune diseases (2024) · cites this paper as [37]
The section 'Regulation of T cell responses by immune checkpoint receptors' (page unavailable) reports that CTLA-4 or PD-1 deficiency can lead to autoimmunity. The Introduction and 'Leveraging biomarkers, pharmacogenomics, and GWAS to predict therapy response and irAEs' (pages unavailable) say checkpoint blockade can cause immune-related adverse events through disrupted tolerance, but do not establish that it exacerbates pre-existing autoimmune diseases. (LLM, conf=0.82)
Experimental — accuracy not yet measuredA dominant role for exhausted autoantigen-specific T cells in AID patients is at odds with the current view of pro-inflammatory activated T cells driving chronic autoimmunity.
“A dominant role for exhausted autoantigen-specific T cells in AID patients is at odds with the current view of pro-inflammatory activated T cells driving chronic autoimmunity. 37”
From Autoantigen-specific CD4+ T cells acquire an exhausted phenotype and persist in human antigen-specific autoimmune diseases (2024) · cites this paper as [37]
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Flagged first, then by citations
Research works printed but not linked: 1
- [44]Borghans JAM, Keşmir C, De Boer RJ. MHC diversity in Individuals and Populations. In: Flower D, Timmis J, editors. In Silico Immunology. Boston, MA: Springer US; 2007. p. 177– 95.
Cited by
Sorted by citations
Saggau, C., Bacher, P., Esser, D., Rasa, M., Meise, S., Mohr, N., Kohlstedt, N., Hutloff, A., Schacht, S.-S., Dargvainiene, J., et al. (2024) · Immunity · doi:10.1016/j.immuni.2024.08.005 · Cited by 79 · see citing works
- Authors
- Mangani, D., Yang, D., & Anderson, A. C.
- Affiliations
- Harvard University (US)
- Corresponding author
- Mangani, Davide
- Anderson, Ana C.
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 2023-02
- Volume
- 56
- Issue
- 2
- Pages
- 256-271
- ISSN
- 1074-7613 (ISSN-L)
- PMC
- PMC9986833
- OpenAlex
- W4320730787
- Cited by
- 33
- References
- 210
- Citations by year
- 2026: 6 · 2025: 11 · 2024: 12 · 2023: 4
- FWCI
- 0.92
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 476 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Immunity (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Melanoma Research Alliance (824733)
- Brigham and Women's Hospital
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (183910)
- National Institutes of Health
- National Cancer Institute (P01CA236749, R01CA229400, R01CA187975, R01CA246653)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
- Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
- Keywords
- autoimmunity, cancer immunotherapy, T cell tolerance, immune checkpoint blockade, T cell dysfunction, autoreactive T cells, antitumor immunity, immunotherapy toxicity management
- MeSH terms
- Autoimmune Diseases, Humans, Immune Tolerance, Neoplasms, T-Lymphocytes, Autoimmunity, Self Tolerance
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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