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Портал Begell Электронная Бибилиотека e-Книги Журналы Справочники и Сборники статей Коллекции
Critical Reviews™ in Immunology
Импакт фактор: 1.352 5-летний Импакт фактор: 3.347 SJR: 1.022 SNIP: 0.55 CiteScore™: 2.19

ISSN Печать: 1040-8401
ISSN Онлайн: 2162-6472

Выпуски:
Том 39, 2019 Том 38, 2018 Том 37, 2017 Том 36, 2016 Том 35, 2015 Том 34, 2014 Том 33, 2013 Том 32, 2012 Том 31, 2011 Том 30, 2010 Том 29, 2009 Том 28, 2008 Том 27, 2007 Том 26, 2006 Том 25, 2005 Том 24, 2004 Том 23, 2003 Том 22, 2002 Том 21, 2001 Том 20, 2000 Том 19, 1999 Том 18, 1998 Том 17, 1997 Том 16, 1996 Том 15, 1995 Том 14, 1994

Critical Reviews™ in Immunology

DOI: 10.1615/CritRevImmunol.2018026335
pages 453-470

IL-33 in Tumor Immunity: Nothing to Sneeze At

Donye Dominguez
Robert H. Lurie Comprehensive Cancer Center, Department of Medicine–Division of Hematology/Oncology, Northwestern University Feinberg School of Medicine, Chicago, Illinois; Biotherapy Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China
Yi Zhang
Biotherapy Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China
Bin Zhang
Robert H. Lurie Comprehensive Cancer Center, Department of Medicine–Division of Hematology/Oncology, Northwestern University Feinberg School of Medicine, Chicago, Illinois; Biotherapy Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China

Краткое описание

Although immunotherapy has been at the forefront of cancer therapy for the last several years, better clinical responses are still desired. Interleukin-33 is perhaps one of the most overlooked antitumor cytokines. Its ability to promote type 1 immune responses, which control tumor growth in preclinical animal models is overshadowed by its association with type 2 immunity and poor prognosis in some human cancers. Accumulating evidence shows that IL-33 is a powerful new tool for restoring and enhancing the body's natural antitumor immunity cycle. Furthermore, the antitumor mechanisms of IL-33 are two-fold, as it can directly boost CD8+ T cell function and restore dendritic cell dysfunction in vivo. Mechanistic studies have identified a novel pathway induced by IL-33 and its receptor ST2 in which dendritic cells avoid dysfunction and retain cross-priming abilities in tumor-bearing conditions. Here, we also comment on IL-33 data in human cancers and explore the idea that endogenous IL-33 may not deserve its reputation for promoting tumor growth. In fact, tumors may hijack the IL-33/ST2 axis to avoid immune surveillance and escape antitumor immunity.

Ключевые слова: IL-33, ST2, CD8+ T cells, dendritic cells, antitumor immunity

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