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Review
. 2019 Jul 16;51(1):15-26.
doi: 10.1016/j.immuni.2019.06.021.

Pas de Deux: Control of Anti-tumor Immunity by Cancer-Associated Inflammation

Affiliations
Review

Pas de Deux: Control of Anti-tumor Immunity by Cancer-Associated Inflammation

"V体育平台登录" Shabnam Shalapour et al. Immunity. .

Abstract

In many settings, tumor-associated inflammation, supported mainly by innate immune cells, contributes to tumor growth VSports手机版. Initial innate activation triggers secretion of inflammatory, regenerative, and anti-inflammatory cytokines, which in turn shape the adaptive immune response to the tumor. Here, we review the current understanding of the intricate dialog between cancer-associated inflammation and anti-tumor immunity. We discuss the changing nature of these interactions during tumor progression and the impact of the tissue environment on the anti-tumor immune response. In this context, we outline important gaps in current understanding by considering basic research and findings in the clinic. The future of cancer immunotherapy and its utility depend on improved understanding of these interactions and the ability to manipulate them in a predictable and beneficial manner. .

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DECLARATION OF INTERESTS

The authors declare no competing interests.

Figures

Figure 1:
Figure 1:. GRAND PAS DE DEUX: Inflammation, Immunity, and Cancer
A schematic description of how cancer-associated inflammation develops, interacts with and modulates anti-tumor immunity. Importantly, inflammation can be either immunosuppressive or immunosupportive. For instance, the extent of myofibroblast activation and TGFβ production can tilt the inflammatory response in a more immunosuppressive direction.
Figure 2:
Figure 2:. Inflammation in the early stages of cancer.
Stress, cell death, obesity, bacterial infection and translocation of microbial components across disrupted barriers induce innate immune cell activation and increased expression of chemokines and cytokines that promote infiltration of adaptive immune cells to the site of tissue stress or injury. Moreover, myeloid cells, especially DC, take up antigens and present them to T cells to induce CTL activation. Despite increasing antigen release, cell death can also be immunosuppressive and tolerogenic, thereby suppressing CTL activation. In a similar manner, monocytes and macrophages can suppress CTL-mediated tumor rejection through expression of IL-10, ARG1, IDO, and TGFβ.
Figure 3:
Figure 3:. Role of Hematopoietic Cells, Particularly Adaptive Immune Cells in Anti-Tumor Immunity in Inflamed TME.
A) Development of different Th cell subsets in the context of an inflammatory tumor environment. Inflammation supports inhibitors of CTL activation and impairs CTL activators. B) Humoral immunity- good or bad? By-and-large, humoral immunity can suppress CTL activation and thereby support tumor growth, but it can also facilitate NK cell activation, through antibody-mediated cytotoxicity and thereby enhancing anti-tumor immunity.
Figure 4:
Figure 4:. Role of Non-hematopoietic Cells in Anti-Tumor Immunity in the Inflamed TME.
A) Immune cell exclusion by CAFs. B) Angiogenesis and lymphangiogenesis; building the road for tumor and immune cell trafficking. C) Cancer cell re-programming, EMT.

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