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T-cell cross-reactivity may explain the large variation in how cancer patients respond to checkpoint inhibitors
1Department of Cancer Immunology, Oslo University Hospital, The Norwegian Radium Hospital, Montebello, Oslo, Norway.
Abstract:
The therapeutic use of the immune system to specifically attack tumours has been a long-standing vision among tumour immunologists. Recently, the use of checkpoint inhibitors to turn-off immunosuppressive signals has proven to be effective in enhancing T-cell reactivity against patient-specific neoantigens, resulting from somatic mutations. Several of the identified T-cell epitopes share similarity with common bacterial and viral antigens, suggesting the involvement of pre-existing microbial cross-reactive T cells in rapid and durable tumour regression seen in some patients. This notion of T-cell cross-reactivity is further supported by the findings that intestinal bacteria can influence checkpoint-blockade therapy. Moreover, early data indicate the presence of such T cells in long-term survival breast cancer patients. This review highlights the main challenges for cancer immunotherapy and discusses the potential contribution of T-cell cross-reactivity in cancer immunotherapy and whether it can be used as a biomarker to predict the responsiveness to checkpoint inhibitors.
Insights
T-cell cross-reactivity, potentially primed by microbes, may enhance cancer immunotherapy responses. This review explores its role and potential as a biomarker for checkpoint inhibitor effectiveness.
Area of Science:
- Immunology
- Oncology
- Microbiology
Background:
- Cancer immunotherapy aims to harness the immune system against tumors.
- Checkpoint inhibitors enhance T-cell responses against tumor neoantigens.
- Microbial antigens may share similarities with tumor neoantigens, suggesting cross-reactivity.
Purpose of the Study:
- To review challenges in cancer immunotherapy.
- To discuss the role of T-cell cross-reactivity in immunotherapy.
- To explore T-cell cross-reactivity as a predictive biomarker for checkpoint inhibitor therapy.
Main Methods:
- Literature review of cancer immunotherapy and T-cell cross-reactivity.
- Analysis of studies on neoantigens, microbial antigens, and T-cell responses.
- Examination of data linking gut microbiota to immunotherapy outcomes.
Main Results:
- T-cell epitopes can resemble microbial antigens, implying cross-reactive T cells.
- Intestinal bacteria influence checkpoint inhibitor therapy efficacy.
- T-cell cross-reactivity is observed in long-term breast cancer survivors.
Conclusions:
- T-cell cross-reactivity is a significant factor in cancer immunotherapy.
- Microbial-induced T-cell cross-reactivity may drive durable tumor regression.
- T-cell cross-reactivity holds promise as a biomarker for predicting immunotherapy response.
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