Expression of Th1/Th2 cytokines in intestinal mucosa of ulcerative colitis

Cui, Hao; Chen, Cun-Long; Yang, Yujie; Zhang, Zuo-Jian; Zhang, Yaodong; Cui, Yao-Sheng

doi:10.11569/wcjd.v11.i10.1524

Cited by 1 publication

(1 citation statement)

References 27 publications

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“…Several gut-derived microbial pathogens were detected inside human tumor tissues of the digestive organs, such as colon, liver, and pancreas recently, promoting cancer progression and resistance to antitumor therapies (Bullman et al, 2017;Kimura et al, 1980;Yazawa et al, 2001). Bifidobacterium is a commensal anaerobic bacteria that can benefit the conventional treatment of ulcerative colitis and has recently been reported as one functional gut microbiota facilitating PDL1-based immunotherapy via improving the function of DCs (Cui et al, 2003;Furrie et al, 2005;Matson et al, 2018;Sivan et al, 2015;Zitvogel et al, 2018). But how and where Bifidobacterium is required for enhancing immunity was not well defined.…”

Section: Resultsmentioning

confidence: 99%

Intratumoral accumulation of gut microbiota facilitates CD47-based immunotherapy via STING signaling

Shi

Zheng

Yang

et al. 2020

Journal of Experimental Medicine

233

189

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Most studies focus on how intestinal microbiota influence cancer immunotherapy through activating gut immunity. However, immunotherapies related to innate responses such as CD47 blockade rely on the rapid immune responses within the tumor microenvironment. Using one defined anaerobic gut microbiota to track whether microbiota interact with host immunity, we observed that Bifidobacterium facilitates local anti-CD47 immunotherapy on tumor tissues through the capacity to accumulate within the tumor microenvironment. Systemic administration of Bifidobacterium leads to its accumulation within the tumor and converts the nonresponder mice into responders to anti-CD47 immunotherapy in a stimulator of interferon genes (STING)– and interferon-dependent fashion. Local delivery of Bifidobacterium potently stimulates STING signaling and increases cross-priming of dendritic cells after anti-CD47 treatment. Our study identifies the mechanism by which gut microbiota preferentially colonize in tumor sites and facilitate immunotherapy via STING signaling.

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