Targeting interleukin-22 for cancer therapy

• Published in: Human vaccines & immunotherapeutics Vol. 14; no. 8; pp. 2012 - 2015
• Main Authors: Markota, Anamarija, Endres, Stefan, Kobold, Sebastian
• Format: Journal Article
• Language: English
• Published: United States Taylor & Francis 01-01-2018; Taylor & Francis Group
• Subjects: Antineoplastic Agents, Immunological - pharmacology; Antineoplastic Agents, Immunological - therapeutic use; cancer immunotherapy; Carcinogenesis - immunology; Drug Development; Humans; interleukin-1; Interleukin-22; Interleukins - antagonists & inhibitors; Interleukins - immunology; Interleukins - metabolism; Molecular Targeted Therapy - methods; Neoplasms - drug therapy; Neoplasms - immunology; Receptors, Interleukin - immunology; Receptors, Interleukin - metabolism; Signal Transduction - drug effects; Signal Transduction - immunology; T-Lymphocytes - immunology; T-Lymphocytes - metabolism; Tumor Microenvironment - drug effects; Tumor Microenvironment - immunology; interleukin-22; interleukin-1; cancer immunotherapy
• ISSN: 2164-5515; 2164-554X
• DOI: 10.1080/21645515.2018.1461300

Interleukin-22 (IL-22) is a member of IL-10 family of cytokines. IL-22 induces proliferative and anti-apoptotic signaling pathways and production of anti-microbial molecules that enhance tissue regeneration and host defense. IL-22 has also been identified as a cancer-promoting cytokine since deregulation of the IL-22-IL-22R1 system is linked to different cancer entities including lung, breast, gastric, pancreatic and colon cancers. T cells and innate lymphoid cells are the main cellular sources of IL-22. Expression of its specific receptor IL-22R1 is restricted to the non-hematopoietic cells which makes the IL-22-IL-22R1 pathway an attractive target for anti-cancer therapy. For development of such therapies, a better understanding of IL-22 regulation in the tumor microenvironment is needed. We could recently decipher how cancer cells promote IL-22 production by memory T cells via induction of IL-1. Here we will discuss how this knowledge might contribute to developing therapies disregulating the IL-22 pathway for cancer immunotherapy.