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Best Pract Res Clin Gastroenterol. 2015 Jun;29(3):425-35. doi: 10.1016/j.bpg.2015.05.001. Epub 2015 May 11.

Innate immunity: actuating the gears of celiac disease pathogenesis.

Author information

1
Committee on Immunology, University of Chicago, Chicago, IL 60637, USA; Department of Medicine, University of Chicago, Chicago, IL 60637, USA. Electronic address: sangman@uchicago.edu.
2
Committee on Immunology, University of Chicago, Chicago, IL 60637, USA; Department of Medicine, University of Chicago, Chicago, IL 60637, USA. Electronic address: stilltoufic@uchicago.edu.
3
Committee on Immunology, University of Chicago, Chicago, IL 60637, USA; Department of Medicine, University of Chicago, Chicago, IL 60637, USA; Department of Pathology, University of Chicago, Chicago, IL 60637, USA; Department of Pediatrics, University of Chicago, Chicago, IL 60637, USA. Electronic address: bjabri@bsd.uchicago.edu.

Abstract

Celiac disease is a T cell mediated immune disorder characterized by the loss of oral tolerance to dietary gluten and the licensing of intraepithelial lymphocytes to kill intestinal epithelial cells, leading to villous atrophy. Innate immunity plays a critical role in both of these processes and cytokines such as interleukin-15 and interferon-α can modulate innate processes such as polarization of dendritic cells as well as intraepithelial lymphocyte function. These cytokines can be modulated by host microbiota, which can also influence dendritic cell function and intraepithelial lymphocyte homeostasis. We will elaborate on the role of interleukin-15, interferon-α, and the microbiota in modulating the processes that lead to loss of tolerance to gluten and tissue destruction in celiac disease.

KEYWORDS:

Celiac disease; Dysbiosis; Immune tolerance; Innate immunity; Interferons; Interleukin-15; Microbiota

PMID:
26060107
PMCID:
PMC4465077
DOI:
10.1016/j.bpg.2015.05.001
[Indexed for MEDLINE]
Free PMC Article

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