2017
DOI: 10.1007/s10620-017-4692-x
|View full text |Cite
|
Sign up to set email alerts
|

Th1 Pathway: The Missing Link Between Inflammatory Bowel Disease and Microscopic Colitis?

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
3
1

Citation Types

0
9
0

Year Published

2018
2018
2022
2022

Publication Types

Select...
7

Relationship

0
7

Authors

Journals

citations
Cited by 10 publications
(9 citation statements)
references
References 16 publications
0
9
0
Order By: Relevance
“…A few investigators have suggested that microscopic colitis may represent an attenuated form of IBD with transformation to "classical" IBD occurring in a subgroup of patients. [1][2][3] This hypothesis is supported by several lines of evidence. First, the gut microbiome in microscopic colitis is characterized by decreased diversity and marked dysbiosis, 4 similar to that of the gut microbiome in CD and UC.…”
mentioning
confidence: 62%
See 2 more Smart Citations
“…A few investigators have suggested that microscopic colitis may represent an attenuated form of IBD with transformation to "classical" IBD occurring in a subgroup of patients. [1][2][3] This hypothesis is supported by several lines of evidence. First, the gut microbiome in microscopic colitis is characterized by decreased diversity and marked dysbiosis, 4 similar to that of the gut microbiome in CD and UC.…”
mentioning
confidence: 62%
“…Beyond a number of published case reports and caseseries, 1,8,10 no prior study has systematically examined the relationship between microscopic colitis and risk of incident IBD. Nevertheless, 2 previous studies attempted to examine cases of IBD diagnosed in cohorts of patients with microscopic colitis.…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…Our results indicated that compared with the control group, levels of Th1 (CD4 + /IFN-γ + ) and Th17 cells (CD4 + /IL-17A + ) in the MLN of RTX-treated mice were significantly increased ( Figure 2 ). Th1 cells promote the cell-mediated inflammatory response by inducing the activation of macrophages, NK cells, and B cells ( Carrasco and Fernández-Bañares, 2017 ). Most of the effector capacity of Th17 cells comes from the fact that IL-17, together with TNF-α, strongly promote inflammation by inducing the expression of adhesion molecules, proinflammatory cytokines (e.g., IL-6, GM-CSF, and G-CSF), chemokines, prostaglandin E2 and matrix metalloproteinases ( Kumawat et al, 2013 ; Rauber et al, 2017 ).…”
Section: Resultsmentioning
confidence: 99%
“…Permeability is also increased by non-steroidal anti-inflammatory drugs and proton-pump inhibitors, common MC triggers, that allow antigens to pass into the lamina propria provoking lymphocytosis [2]. Increased expression of TNF-α, interferon-γ, and the Th1-specific transcription factor T-BET in patients with MC who eventually developed IBD suggests a common immunological pathophysiological pathway in the MC-to-IBD transformation [3,10]. Few studies found associations between human leukocyte antigen haplotypes, DQ2 and DQ8, and risk of CC, LC, and IBD development [11][12][13][14][15].…”
Section: Discussionmentioning
confidence: 99%