Abo Bibliothek: Guest
Digitales Portal Digitale Bibliothek eBooks Zeitschriften Referenzen und Berichte Forschungssammlungen
Critical Reviews™ in Immunology
Impact-faktor: 1.352 5-jähriger Impact-Faktor: 3.347 SJR: 1.022 SNIP: 0.55 CiteScore™: 2.19

ISSN Druckformat: 1040-8401
ISSN Online: 2162-6472

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

ABSTRAKT

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.


Articles with similar content:

Regulation of Immune Responses of the Intestinal Mucosa
Critical Reviews™ in Immunology, Vol.16, 1996, issue 3
Stephan R. Targan, Maria T. Abreu-Martin
Peripheral Nonresponsiveness to Orally Administered Soluble Protein Antigens
Critical Reviews™ in Immunology, Vol.21, 2001, issue 1-3
Hai Ning Shi, Cathryn Nagler-Anderson
Tumor Antigen Presentation by Dendritic Cells
Critical Reviews™ in Immunology, Vol.30, 2010, issue 4
Nina Dickgreber, Ian F. Hermans, Troels R. Petersen
T-Cell Adoptive Therapy of Tumors: Mechanisms of Improved Therapeutic Performance
Critical Reviews™ in Immunology, Vol.21, 2001, issue 1-3
Brian J. Czerniecki, Jorgen Kjaergaard, Liaomin Peng, Peter A. Cohen, Gary K. Koski, James H. Finke, Suyu Shu, Gregory E. Plautz
CD4+ T Cells in Adoptive Immunotherapy and the Indirect Mechanism of Tumor Rejection
Critical Reviews™ in Immunology, Vol.20, 2000, issue 1
Liaomin Peng, David E. Weng, Peter A. Cohen, Suyu Shu, Julian A. Kim, Gregory E. Plautz