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von Roemeling, Christina A; Wang, Yifan; Qie, Yaqing; Yuan, Hengfeng; Zhao, Hai; Liu, Xiujie; Yang, Zhaogang; Yang, Mingming; Deng, Weiye; Bruno, Katelyn A; Chan, Charles K; Lee, Andrew S; Rosenfeld, Stephen S; Yun, Kyuson; Johnson, Aaron J; Mitchell, Duane A; Jiang, Wen; Kim, Betty Y S
Nature communications, 03/2020, Letnik: 11, Številka: 1Journal Article
Tumour cell phagocytosis by antigen presenting cells (APCs) is critical to the generation of antitumour immunity. However, cancer cells can evade phagocytosis by upregulating anti-phagocytosis molecule CD47. Here, we show that CD47 blockade alone is inefficient in stimulating glioma cell phagocytosis. However, combining CD47 blockade with temozolomide results in a significant pro-phagocytosis effect due to the latter's ability to induce endoplasmic reticulum stress response. Increased tumour cell phagocytosis subsequently enhances antigen cross-presentation and activation of cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) in APCs, resulting in more efficient T cell priming. This bridging of innate and adaptive responses inhibits glioma growth, but also activates immune checkpoint. Sequential administration of an anti-PD1 antibody overcomes this potential adaptive resistance. Together, these findings reveal a dynamic relationship between innate and adaptive immune regulation in tumours and support further investigation of phagocytosis modulation as a strategy to enhance cancer immunotherapy responses.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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in: SICRIS
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