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. 2021 Jun 23;13:107. doi: 10.1186/s13073-021-00923-w

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© The Author(s) 2021

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — The intestinal microbiome may help determine outcomes of ICI therapy. Increased intestinal microbiome diversity and the presense of specific intestinal bacteria are associated with both responses and toxicity following ICI therapy. One possible group of mechanisms is antigen-independent, via induction of mucosal and systemic immune responses, especially Th1 and cytotoxic T cell responses, by the microbiome (left). Alternatively, antigen-specific mechanisms, specifically antigen mimicry between microbial and tumor antigens, could modulate anti-tumor immune responses. For example, T cell targeting an epitope SVYRYYGL (SVY) expressed in Bifidobacterium breve cross-react with a model neoantigen, SIYRYYGL (SIY) [63]. Antigen-specific T cells that can cross-react against both commensal bacterial and tumor antigens may play a role in ICI therapy (right)