Immunology of Crohn's Disease

@article{Braat2006ImmunologyOC,
  title={Immunology of Crohn's Disease},
  author={Henri Braat and Maikel Petrus Peppelenbosch and Daniel W. Hommes},
  journal={Annals of the New York Academy of Sciences},
  year={2006},
  volume={1072}
}
Abstract:  The immense microbiological load of the gastrointestinal tract poses a daunting challenge for the mucosal immune system: whereas it should tolerate the vast number of commensal bacteria, it should adequately attack pathogenic organisms. Millions of years of co‐evolution have produced an intricate system in which interactions between the endogenous flora and mucosal immune system manage to perform this difficult balancing act. When components of this interaction are defective, for… 
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References

SHOWING 1-10 OF 132 REFERENCES
The immunological and genetic basis of inflammatory bowel disease
TLDR
The most important finding is the identification of mutations in the gene that encodes NOD2 (nucleotide-binding oligomerization domain 2) protein in a subgroup of patients with Crohn's disease.
Therapeutic manipulation of the enteric microflora in inflammatory bowel diseases: antibiotics, probiotics, and prebiotics.
  • R. Sartor
  • Medicine, Biology
    Gastroenterology
  • 2004
TLDR
Current clinical trials do not fulfill evidence-based criteria for using these agents in inflammatory bowel diseases (IBD), but multiple nonrigorous studies and widespread clinical experience suggest that metronidazole and/or ciprofloxacin can treat Crohn's colitis and ileocolitis, whereas selected probiotic preparations prevent relapse of quiescent ulcerativecolitis and relapsing pouchitis.
Role of the faecal stream in the maintenance of Crohn's colitis.
TLDR
Results suggest that factors greater than 0.22 microns in the faecal stream are responsible for the maintenance and exacerbation of inflammation in Crohn's disease.
Nod2-Dependent Regulation of Innate and Adaptive Immunity in the Intestinal Tract
TLDR
It is shown that protective immunity mediated by Nod2 recognition of bacterial muramyl dipeptide is abolished in Nod1-deficient mice, providing a possible mechanism for Nod 2 mutations in CD.
A primitive T cell-independent mechanism of intestinal mucosal IgA responses to commensal bacteria.
TLDR
The IgA against intestinal commensal bacterial antigens was analyzed; it was not simply "natural antibody" but was specifically induced and responded to antigenic changes within an established gut flora.
Type 1 T-helper cell predominance and interleukin-12 expression in the gut of patients with Crohn's disease.
TLDR
It is suggested that a critical event in the initiation of bowel inflammatory lesions in CD may involve up-regulation of IL-12 production, resulting in conditions that maximally promote type 1 T-helper immune responses.
Mucosal flora in inflammatory bowel disease.
TLDR
It is hypothesized that the healthy mucosa is capable of holding back fecal bacteria and that this function is profoundly disturbed in patients with IBD, suggesting that the changes in the mucosal flora in IBD are not secondary to inflammation, but a result of a specific host response.
Crohn's disease and the NOD2 gene: a role for paneth cells.
...
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