Journal
IMMUNOTHERAPY
Volume 14, Issue 6, Pages 459-473Publisher
FUTURE MEDICINE LTD
DOI: 10.2217/imt-2021-0228
Keywords
antitumor effect; chemokine; chemokine receptor; chemotactic functions; chimeric antigen receptor; immunosuppressive tumor microenvironment; infiltration; solid tumor; trafficking
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Funding
- Post-Doctor Research Project, West China Hospital, Sichuan University [2020HXBH124]
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Immunotherapy with immune checkpoint inhibitors has shown great success in cancer treatment. However, its effectiveness in solid tumors is limited and varies among patients. Researchers are therefore searching for ways to improve the efficacy of immune checkpoint inhibitors and predict patient response. Biomarkers such as CD31, a marker for tumor neovasculature, may help predict tumor sensitivity to immune checkpoint inhibitors.
Plain language summary Chimeric antigen receptor T (CAR-T) cell therapy is emerging as a promising therapeutic approach for cancers in the blood. The success of CAR-T cells has also sparked interest in applying this strategy to solid tumors; however, attempts have been disappointing, with only a few patients achieving a partial response. The chemokine/chemokine receptor axis plays a key role in the growth and spread of tumors. Unfortunately, chemokines and chemokine receptors in immune cells and the environment surrounding the tumor do not always match, which results in inefficient immune cell trafficking and infiltration. Therefore, reversing the 'mismatch' of chemokines and chemokine receptors appears to be a promising method for potential treatment. In this review, we discuss functions of the chemokine/chemokine receptor axis in cancer immunity and the current understanding, challenges and prospects for improving CAR-T cell therapy by reversing this mismatch. Currently, the antitumor efficacy of chimeric antigen receptor T cells in solid tumors is modest. Both chemokines and their receptors play a key role in the proliferation of cancer cells, tumor angiogenesis, organ-selective metastasis and migration of immune cells to solid tumors. Unfortunately, frequent chemokine/chemokine receptor 'mismatch' between effector cells and the tumor microenvironment results in inefficient T-cell infiltration and antitumor efficacy. Thus, reversing the 'mismatch' of chemokines and chemokine receptors appears to be a promising method for promoting T-cell infiltration into the tumor and enhancing their antitumor efficacy. In this review, we discuss functions of the chemokine/chemokine receptor axis in cancer immunity and the current understanding, challenges and prospects for improving the effect of chimeric antigen receptor T cells by reversing the mismatch between chemokines and chemokine receptors.
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