scholarly journals Connecting the dots from Toll-like receptors to innate immune cells and inflammatory bowel disease

2003 ◽  
Vol 111 (9) ◽  
pp. 1284-1286 ◽  
Author(s):  
David L. Boone ◽  
Averil Ma
Keyword(s):  
Inflammatory Bowel Disease ◽  
Immune Cells ◽  
Bowel Disease ◽  
Innate Immune ◽  
Innate Immune Cells ◽  
Toll Like Receptors ◽  
Inflammatory Bowel ◽  
Connecting The Dots

scholarly journals Impact of Autophagy of Innate Immune Cells on Inflammatory Bowel Disease

Cells ◽  
2018 ◽  
Vol 8 (1) ◽  
pp. 7 ◽  
Author(s):  
Tomoya Iida ◽  
Yoshihiro Yokoyama ◽  
Kohei Wagatsuma ◽  
Daisuke Hirayama ◽  
Hiroshi Nakase
Keyword(s):  
Inflammatory Bowel Disease ◽  
Immune Response ◽  
Innate Immune Response ◽  
Immune Cells ◽  
Bowel Disease ◽  
Innate Immune ◽  
Unknown Etiology ◽  
Innate Immune Cells ◽  
Enhanced Production ◽  
Inflammatory Bowel

Autophagy, an intracellular degradation mechanism, has many immunological functions and is a constitutive process necessary for maintaining cellular homeostasis and organ structure. One of the functions of autophagy is to control the innate immune response. Many studies conducted in recent years have revealed the contribution of autophagy to the innate immune response, and relationships between this process and various diseases have been reported. Inflammatory bowel disease is an intractable disorder with unknown etiology; however, immunological abnormalities in the intestines are known to be involved in the pathology of inflammatory bowel disease, as is dysfunction of autophagy. In Crohn’s disease, many associations with autophagy-related genes, such as ATG16L1, IRGM, NOD2, and others, have been reported. Abnormalities in the ATG16L1 gene, in particular, have been reported to cause autophagic dysfunction, resulting in enhanced production of inflammatory cytokines by macrophages as well as abnormal function of Paneth cells, which are important in intestinal innate immunity. In this review, we provide an overview of the autophagy mechanism in innate immune cells in inflammatory bowel disease.

scholarly journals Association Between Toll-Like Receptors/CD14 Gene Polymorphisms and Inflammatory Bowel Disease in Korean Population

2012 ◽  
Vol 27 (1) ◽  
pp. 72 ◽  
Author(s):  
Eun Jung Kim ◽  
Woo Chul Chung ◽  
Kang-Moon Lee ◽  
Chang Nyol Paik ◽  
Sung Hoon Jung ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Gene Polymorphisms ◽  
Korean Population ◽  
Toll Like Receptors ◽  
Inflammatory Bowel ◽  
Cd14 Gene

Analysis of toll-like receptors 2, 4 and MD2 in inflamed and non-inflamed gut tissues in inflammatory bowel disease

2004 ◽  
Vol 200 (4) ◽  
pp. 321
Author(s):  
F. Autschbach ◽  
T. Giese ◽  
N. Gassler ◽  
I. Berger ◽  
B. Sido ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Toll Like Receptors ◽  
Inflammatory Bowel

scholarly journals P031 EXPRESSION OF TOLL-LIKE RECEPTORS 2, 3 AND 4 IN CHILDREN WITH INFLAMMATORY BOWEL DISEASE

2007 ◽  
Vol 1 (1) ◽  
pp. 12
Author(s):  
G. Veres ◽  
B. Szebeni ◽  
M. Mraz ◽  
A. Dezsõfi ◽  
A. Vannay ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Toll Like Receptors ◽  
Inflammatory Bowel

scholarly journals Histamine Receptor 2 is Required to Suppress Innate Immune Responses to Bacterial Ligands in Patients with Inflammatory Bowel Disease

2016 ◽  
Vol 22 (7) ◽  
pp. 1575-1586 ◽  
Author(s):  
Sylwia Smolinska ◽  
David Groeger ◽  
Noelia Rodriguez Perez ◽  
Elisa Schiavi ◽  
Ruth Ferstl ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Immune Responses ◽  
Bowel Disease ◽  
Histamine Receptor ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Inflammatory Bowel

Extra-articular manifestations: inflammatory bowel disease

2016 ◽  
Author(s):  
Dirk Elewaut ◽  
Heleen Cypers ◽  
Matthew L. Stoll ◽  
Charles O. Elson
Keyword(s):  
Inflammatory Bowel Disease ◽  
Intestinal Microbiota ◽  
Bowel Disease ◽  
Intestinal Barrier ◽  
Innate Immune ◽  
Intestinal Barrier Function ◽  
Innate Immune Responses ◽  
Susceptible Host ◽  
Inflammatory Bowel

A significant overlap exists between spondyloarthritis (SpA) and inflammatory bowel disease (IBD), particularly in the IL-23/IL-17 pathway. Shared immunologic mechanisms include aberrant innate immune responses, an excess of Th1/Th17-mediated immunity, and inadequate immune regulation. Many genetic factors associated with IBD are involved in host–pathogen interactions and intestinal barrier function, and the intestinal microbiota do appear to play an important role in disease development. Hence the current hypothesis for IBD pathogenesis is that it stems from a dysregulated immune response to intestinal microbiota in a genetically susceptible host. In SpA, evidence for a role of intestinal microbiota is less abundant, but given the overlap with IBD, it is plausible that gut microbiota are important players in SpA pathogenesis as well. However, there are significant genetic differences between these two conditions, as well as differing responses to biologic therapy.

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