This is a second paper in this series (microbiota and immunotherapy). This study came from Thomas Gajewski's lab. It showed that cancer growth or effectiveness of anti-PD-L1 anti-cancer immunotherapy were influenced by composition of gut microflora, more specifically by presence of Bifidobacterium.
Now this paper starts with experimental results that became classical experiments in gut immunology [since the discovery of TH17 subset]. Namely, the authors showed that B6 black mouse colonies derived from JAX lab or Taconic showed different susceptibility to cancer growth.
This difference between JAX and Taconic mice disappeared when mice were co-housed, implying the role of gut microflora.
This hypothesis was confirmed in fecal cross-feeding experiments between JAX and Tac mice. It turned out that gut microbiota from JAX mice could enhance anti-tumor immunity when transplanted into Tac mice [but not vise versa].
Furthermore, JAX mouse microbiota could enhance anti-cancer effectiveness of anti-PD-L1 immunotherapy.
Finally, the authors found that a single commensal species, called Bifidobacterium, was largely responsible for microbiota's effect on cancer immunity.
In summary, the authors proposed that live Bifidobacterium could enhance anti-cancer immunity by supporting "generic" dendritic cell maturation and improving T cells antigen-sensitivity.
This model, however, lacks data that could meaningfully explain why and how only Bifidobacterium has such influence on anti-cancer immunity. Also, it would have been more relevant to test FDA approved anti-PD1 antibody here rather than not-yet-approved anti-PD-L1 antibody therapy.