[Durgical](https://durgical.com/en/) › [DurgiPedia](https://durgical.com/en/durgipedia/) › [General pathology](https://durgical.com/en/general-pathology/) › [Neoplasia](https://durgical.com/en/general-pathology/#a-neoplasia) › How tumours evade the immune system [General pathology](https://durgical.com/en/general-pathology/) · [Neoplasia](https://durgical.com/en/general-pathology/#a-neoplasia) # How tumours evade the immune system - Mechanism The immune system can recognise and kill cancer cells. Tumours that survive learn to hide from T cells and to switch them off. Updated 2026-11-01 ## Key points - Immunoediting: elimination, equilibrium, escape. - Hide: loss of MHC class I or of beta-2 microglobulin, loss of the target antigen. - Suppress: PD-L1 on tumour cells binds PD-1 on T cells; CTLA-4 dampens T-cell priming; regulatory T cells, TGF-beta, IL-10, suppressive macrophages. - Hodgkin lymphoma: Reed-Sternberg cells often amplify 9p24.1 (PD-L1/PD-L2), so they respond well to PD-1 blockade. - High mutational burden (melanoma, smoking-related lung cancer, mismatch repair-deficient tumours) means more neoantigens and better responses to checkpoint inhibitors. - Immunosuppression (HIV, transplant) raises virus-driven cancers: Kaposi sarcoma, EBV lymphomas, HPV cancers. ## What it is Cytotoxic T cells recognise tumour antigens (neoantigens from mutated proteins, viral proteins, overexpressed self proteins) and kill tumour cells; NK cells kill cells that lose MHC class I. Through immunoediting, the clones that survive are those that hide (loss of MHC class I or antigen) or actively suppress immunity (PD-L1, regulatory T cells, suppressive cytokines). Blocking these brakes with checkpoint inhibitors is now standard therapy for many cancers. ## Step by step - Tumour cells express abnormal antigens presented on MHC class I. - Dendritic cells cross-present these antigens and prime CD8 T cells in lymph nodes. - Primed T cells reach the tumour and kill antigen-bearing cells; NK cells kill cells lacking MHC class I. - Selection favours clones that lose MHC class I, antigen-processing proteins or the target antigen. - Tumour cells and the microenvironment express PD-L1 and recruit regulatory T cells and suppressive myeloid cells. - Exhausted T cells stop killing; the tumour escapes and grows. ## Tumour escape strategies | Strategy | Mechanism | Clinical counterpart | | --- | --- | --- | | Hide the antigen | Loss of MHC class I, beta-2 microglobulin or antigen | Resistance to checkpoint inhibitors | | [Switch off T cells](https://durgical.com/en/conditions/melanoma/) | PD-L1 binds PD-1 | Anti-PD-1 and anti-PD-L1 antibodies | | Block priming | CTLA-4 competes for B7 on antigen-presenting cells | Anti-CTLA-4 antibodies | | Suppressive environment | Regulatory T cells, TGF-beta, IL-10, suppressive macrophages | Poor T-cell infiltration (cold tumours) | | [Exploit a weak host](https://durgical.com/en/conditions/kaposi-sarcoma/) | HIV or transplant immunosuppression | Kaposi sarcoma, EBV lymphomas, HPV-related cancers | ## Clinical notes - Checkpoint inhibitors are used in melanoma, lung, kidney and many other cancers, and in any mismatch repair-deficient tumour. - Their side effects are immune-related: colitis, hepatitis, pneumonitis, thyroiditis, hypophysitis, dermatitis. - Merkel cell carcinoma, often driven by a polyomavirus, is very immunogenic and responds to PD-1 or PD-L1 blockade. ## Memory aid Tumours escape with an invisibility cloak (no MHC I) and a remote control that turns T cells off (PD-L1); checkpoint drugs take away the remote. ## Test yourself Think of the answer, then tap the question to see it. ## Why do NK cells matter when tumours lose MHC class I? NK cells kill cells lacking MHC class I (missing self), which partly offsets this escape strategy. ## What is the role of PD-L1 on tumour cells? It binds PD-1 on activated T cells and inhibits them, causing T-cell exhaustion. ## Why does Hodgkin lymphoma respond well to PD-1 blockade? Reed-Sternberg cells often amplify 9p24.1, which carries the PD-L1 and PD-L2 genes, so the tumour depends on this brake. ## Why do mismatch repair-deficient tumours respond to checkpoint inhibitors? They carry many mutations, producing many neoantigens that T cells can recognise once released from inhibition. [Add to my cards (4)](https://durgical.app/estudiar/?add=/en/general-pathology/how-tumours-evade-the-immune-system/) ## Related - [The hallmarks of cancer](https://durgical.com/en/general-pathology/the-hallmarks-of-cancer/) - [Genomic instability: mismatch repair, BRCA and xeroderma pigmentosum](https://durgical.com/en/general-pathology/genomic-instability-mismatch-repair-brca-and-xeroderma-pigmentosum/) - [Oncogenic viruses and H. pylori: the table to know](https://durgical.com/en/general-pathology/oncogenic-viruses-and-h-pylori-the-table-to-know/) - [Invasion and metastasis: the metastatic cascade, step by step](https://durgical.com/en/general-pathology/invasion-and-metastasis-the-metastatic-cascade-step-by-step/) ## Related conditions - [Melanoma](https://durgical.com/en/conditions/melanoma/) - [Hodgkin lymphoma](https://durgical.com/en/conditions/hodgkin-lymphoma/) - [Lung cancer](https://durgical.com/en/conditions/lung-cancer/) - [Lynch syndrome (hereditary non-polyposis colorectal cancer)](https://durgical.com/en/conditions/lynch-syndrome/) - [Colorectal cancer](https://durgical.com/en/conditions/colorectal-cancer/) - [Renal cell carcinoma](https://durgical.com/en/conditions/renal-cell-carcinoma/) - [Kaposi sarcoma](https://durgical.com/en/conditions/kaposi-sarcoma/) - [HIV infection and AIDS](https://durgical.com/en/conditions/hiv-infection-and-aids/) - [Merkel cell carcinoma](https://durgical.com/en/conditions/merkel-cell-carcinoma/) - [Cervical cancer](https://durgical.com/en/conditions/cervical-cancer/) ## Elsewhere in DurgiPedia - [Tumor immunology and checkpoint inhibitors](https://durgical.com/en/immunology/tumor-immunology-and-checkpoint-inhibitors/) - [Cancer immunotherapy: checkpoint inhibitors, CAR-T and vaccines](https://durgical.com/en/immunology/cancer-immunotherapy-checkpoint-inhibitors-car-t-and-vaccines/) - [Natural killer cell](https://durgical.com/en/immunology/natural-killer-cell/) - [CD8⁺ cytotoxic T cell](https://durgical.com/en/immunology/cd8-cytotoxic-t-cell/) - [Regulatory T cell (Treg, FOXP3)](https://durgical.com/en/immunology/regulatory-t-cell/) - [MHC/HLA class I and II](https://durgical.com/en/immunology/mhc-hla-class-i-and-ii/) - [Secondary immunodeficiency: HIV, malnutrition, drugs, asplenia](https://durgical.com/en/immunology/secondary-immunodeficiency-hiv-malnutrition-drugs-asplenia/) ## Microorganisms - [Human herpesvirus 8](https://durgical.com/en/microbiology/human-herpesvirus-8/) - [Epstein–Barr virus](https://durgical.com/en/microbiology/epstein-barr-virus/) - [Human papillomavirus](https://durgical.com/en/microbiology/human-papillomavirus/) [← All of general pathology](https://durgical.com/en/general-pathology/) Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given. Sources: [Immune Checkpoint Inhibitors](https://www.cancer.gov/about-cancer/treatment/types/immunotherapy/checkpoint-inhibitors) (National Cancer Institute (NCI), 2026); [Targeted Therapy to Treat Cancer](https://www.cancer.gov/about-cancer/treatment/types/targeted-therapies) (National Cancer Institute (NCI), 2026); [What Is Cancer?](https://www.cancer.gov/about-cancer/understanding/what-is-cancer) (National Cancer Institute (NCI), 2026). ## **Spotted a mistake?** We are always improving for the community. Tell us what is wrong and our team will review it. Report a mistake Representative model, for educational purposes only. --- Source: https://durgical.com/en/general-pathology/how-tumours-evade-the-immune-system/ License: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Cite as: DurgiPedia (durgical.com), https://durgical.com/en/general-pathology/how-tumours-evade-the-immune-system/