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REVIEW: Tumor Necrosis Factor and Lymphotoxin in Regulation of Intestinal Inflammation

E. O. Gubernatorova1 and A. V. Tumanov1,2*

1Institute of Molecular Biology, Russian Academy of Sciences, 119991 Moscow, Russia; E-mail: tumanov@uthscsa.edu

2University of Texas Health Science Center, Department of Microbiology, Immunology, and Molecular Genetics, San Antonio, TX 78229, USA

* To whom correspondence should be addressed.

Received July 3, 2016; Revision received August 16, 2016
Ulcerative colitis and Crohn’s disease are the major forms of inflammatory bowel disease. Cytokines of the tumor necrosis factor (TNF) family play an important role in the regulation of intestinal inflammation. In this review, we discuss the function of key cytokines of this family – TNF and lymphotoxin (LT) – in mucosal healing, IgA production, and in control of innate lymphoid cells (ILCs), novel regulators of mucosal homeostasis in the gut. TNF plays a central role in the pathogenesis of inflammatory bowel diseases (IBD). LT regulates group 3 of ILCs and IL-22 production and protects the epithelium against damage by chemicals and mucosal bacterial pathogens. In addition, we discuss major mouse models employed to study the mechanism of intestinal inflammation, their advantages and limitations, as well as application of TNF blockers in the therapy for IBD.
KEY WORDS: tumor necrosis factor, lymphotoxin, intestinal inflammation, inflammatory bowel disease, mouse models

DOI: 10.1134/S0006297916110092