Abstract |
IL-6 signaling is of central importance for the maintenance of chronic intestinal inflammation in inflammatory bowel diseases (IBD) such as Crohn's disease and ulcerative colitis. IL-6 regulates T cell differentiation, activation and resistance against apoptosis and thereby controls the balance between pro-inflammatory T cell subsets such as Th1 or Th17 cells and immunosuppressive regulatory T cells. Furthermore, IL-6 has been implicated in the pathogenesis of colorectal cancer (CRC). In fact, IL-6 directly promotes tumor cell proliferation and survival through STAT3 activation. Due to its role in both types of diseases, IL-6 has been proposed as a missing link between inflammation and tumor development. During recent years, several therapeutics targeting IL-6 dependent pathways have been developed. Although clinical data about anti-IL-6 treatment in intestinal diseases are currently scarce, targeting this pathway might be a promising strategy in IBD and CRC.
|
Authors | Maximilian J Waldner, Markus F Neurath |
Journal | Seminars in immunology
(Semin Immunol)
Vol. 26
Issue 1
Pg. 75-9
(Feb 2014)
ISSN: 1096-3618 [Electronic] England |
PMID | 24447345
(Publication Type: Journal Article, Review)
|
Copyright | Copyright © 2014 Elsevier Ltd. All rights reserved. |
Chemical References |
- Interleukin-6
- STAT3 Transcription Factor
|
Topics |
- Animals
- Cell Transformation, Neoplastic
(genetics, immunology, metabolism)
- Colorectal Neoplasms
(drug therapy, genetics, immunology, metabolism)
- Gene Expression Regulation
(drug effects)
- Humans
- Inflammatory Bowel Diseases
(drug therapy, genetics, immunology, metabolism)
- Interleukin-6
(genetics, metabolism)
- Molecular Targeted Therapy
- STAT3 Transcription Factor
(metabolism)
- Signal Transduction
(drug effects)
- T-Lymphocyte Subsets
(immunology, metabolism)
|