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Interferon-dependent IL-10 production by Tregs limits tumor Th17 inflammation. | LitMetric

AI Article Synopsis

  • IL-10 and regulatory T cells (Tregs) in tumors can weaken Th1 immune responses, making them important targets for cancer therapies while also suppressing Th17 cells, which are linked to worse cancer outcomes.
  • A study using mouse tumor models showed that activated Tregs are the primary source of IL-10 in the tumor environment, which helps control Th17-related inflammation.
  • The research highlighted that type I interferon (IFN) signaling is crucial for the accumulation and function of IL-10+ Tregs, suggesting that disrupting this signaling pathway could unintentionally enhance Th17 inflammation and promote tumor growth.

Article Abstract

The capacity of IL-10 and Tregs in the inflammatory tumor microenvironment to impair anticancer Th1 immunity makes them attractive targets for cancer immunotherapy. IL-10 and Tregs also suppress Th17 activity, which is associated with poor prognosis in several cancers. However, previous studies have overlooked their potential contribution to the regulation of pathogenic cancer-associated inflammation. In this study, we investigated the origin and function of IL-10–producing cells in the tumor microenvironment using transplantable tumor models in mice. The majority of tumor-associated IL-10 was produced by an activated Treg population. IL-10 production by Tregs was required to restrain Th17-type inflammation. Accumulation of activated IL-10+ Tregs in the tumor required type I IFN signaling but not inflammatory signaling pathways that depend on TLR adapter protein MyD88 or IL-12 family cytokines. IL-10 production limited Th17 cell numbers in both spleen and tumor. However, type I IFN was required to limit Th17 cells specifically in the tumor microenvironment, reflecting selective control of tumor-associated Tregs by type I IFN. Thus, the interplay of type I IFN, Tregs, and IL-10 is required to negatively regulate Th17 inflammation in the tumor microenvironment. Therapeutic interference of this network could therefore have the undesirable consequence of promoting Th17 inflammation and cancer growth.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3809773PMC
http://dx.doi.org/10.1172/JCI65180DOI Listing

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