Hdl Handle:
http://hdl.handle.net/10147/209050
Title:
Crohn's disease.
Authors:
Shanahan, Fergus
Affiliation:
Department of Medicine, Clinical Sciences Building, Cork University Hospital,, Cork, Ireland. F.shanahan@ucc.ie
Citation:
Lancet. 2002 Jan 5;359(9300):62-9.
Journal:
Lancet
Issue Date:
3-Feb-2012
URI:
http://hdl.handle.net/10147/209050
DOI:
10.1016/S0140-6736(02)07284-7
PubMed ID:
11809204
Abstract:
Crohn's disease is a disorder mediated by T lymphocytes which arises in genetically susceptible individuals as a result of a breakdown in the regulatory constraints on mucosal immune responses to enteric bacteria. Regulation of immune reactivity to enteric antigens has improved understanding of the pathophysiological mechanisms of Crohn's disease, and has expanded therapeutic options for patients with this disorder. Disease heterogeneity is probable, with various underlying defects associated with a similar pathophysiological outcome. Although most conventional drug treatments are directed at modification of host response, therapeutic manipulation of the enteric flora is becoming a realistic option.
Language:
eng
MeSH:
Animals; *Carrier Proteins; *Crohn Disease/genetics/immunology/microbiology; Genetic Predisposition to Disease; Humans; Intestines/immunology/microbiology; *Intracellular Signaling Peptides and Proteins; Nod2 Signaling Adaptor Protein; Proteins/genetics
ISSN:
0140-6736 (Print); 0140-6736 (Linking)

Full metadata record

DC FieldValue Language
dc.contributor.authorShanahan, Fergusen_GB
dc.date.accessioned2012-02-03T15:10:55Z-
dc.date.available2012-02-03T15:10:55Z-
dc.date.issued2012-02-03T15:10:55Z-
dc.identifier.citationLancet. 2002 Jan 5;359(9300):62-9.en_GB
dc.identifier.issn0140-6736 (Print)en_GB
dc.identifier.issn0140-6736 (Linking)en_GB
dc.identifier.pmid11809204en_GB
dc.identifier.doi10.1016/S0140-6736(02)07284-7en_GB
dc.identifier.urihttp://hdl.handle.net/10147/209050-
dc.description.abstractCrohn's disease is a disorder mediated by T lymphocytes which arises in genetically susceptible individuals as a result of a breakdown in the regulatory constraints on mucosal immune responses to enteric bacteria. Regulation of immune reactivity to enteric antigens has improved understanding of the pathophysiological mechanisms of Crohn's disease, and has expanded therapeutic options for patients with this disorder. Disease heterogeneity is probable, with various underlying defects associated with a similar pathophysiological outcome. Although most conventional drug treatments are directed at modification of host response, therapeutic manipulation of the enteric flora is becoming a realistic option.en_GB
dc.language.isoengen_GB
dc.subject.meshAnimalsen_GB
dc.subject.mesh*Carrier Proteinsen_GB
dc.subject.mesh*Crohn Disease/genetics/immunology/microbiologyen_GB
dc.subject.meshGenetic Predisposition to Diseaseen_GB
dc.subject.meshHumansen_GB
dc.subject.meshIntestines/immunology/microbiologyen_GB
dc.subject.mesh*Intracellular Signaling Peptides and Proteinsen_GB
dc.subject.meshNod2 Signaling Adaptor Proteinen_GB
dc.subject.meshProteins/geneticsen_GB
dc.titleCrohn's disease.en_GB
dc.contributor.departmentDepartment of Medicine, Clinical Sciences Building, Cork University Hospital,, Cork, Ireland. F.shanahan@ucc.ieen_GB
dc.identifier.journalLanceten_GB
dc.description.provinceMunster-
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