16202223

Source:http://linkedlifedata.com/resource/pubmed/id/16202223

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Subject	Predicate	Object	Context
pubmed-article:16202223	rdf:type	pubmed:Citation	lld:pubmed
pubmed-article:16202223	lifeskim:mentions	umls-concept:C0035820	lld:lifeskim
pubmed-article:16202223	lifeskim:mentions	umls-concept:C0079488	lld:lifeskim
pubmed-article:16202223	lifeskim:mentions	umls-concept:C0030305	lld:lifeskim
pubmed-article:16202223	lifeskim:mentions	umls-concept:C0007028	lld:lifeskim
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pubmed-article:16202223	lifeskim:mentions	umls-concept:C0242943	lld:lifeskim
pubmed-article:16202223	pubmed:issue	3	lld:pubmed
pubmed-article:16202223	pubmed:dateCreated	2005-10-5	lld:pubmed
pubmed-article:16202223	pubmed:abstractText	Autoimmune pancreatitis is a recently defined nosological entity, which accounts for 4.6-6% of all forms of chronic pancreatitis and is often associated with other autoimmune diseases, particularly Sjogren's syndrome. Possession of the HLA DRB10405-DQB10401 genotype confers a risk for the development of autoimmune pancreatitis. Autoantibodies against carbonic anhydrase II and lactoferrin are frequently present in affected subjects and are suspected to have a pathogenic role. A link between gastric infection by Helicobacter pylori and autoimmune pancreatitis has been hypothesized. We used in silico protein analysis and search for HLA binding motifs to verify this hypothesis. We found a significant homology between human carbonic anhydrase II and alpha-carbonic anhydrase of Helicobacter pylori, an enzyme which is fundamental for the survival and proliferation of the bacterium in the gastric environment. Moreover, the homologous segments contain the binding motif of the HLA molecule DRB1*0405. Our data strengthen the hypothesis that gastric Helicobacter pylori infection can trigger autoimmune pancreatitis in genetically predisposed subjects.	lld:pubmed
pubmed-article:16202223	pubmed:language	eng	lld:pubmed
pubmed-article:16202223	pubmed:journal	http://linkedlifedata.com/r...	lld:pubmed
pubmed-article:16202223	pubmed:citationSubset	IM	lld:pubmed
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pubmed-article:16202223	pubmed:status	MEDLINE	lld:pubmed
pubmed-article:16202223	pubmed:issn	1582-1838	lld:pubmed
pubmed-article:16202223	pubmed:author	pubmed-author:BenvengaSS	lld:pubmed
pubmed-article:16202223	pubmed:author	pubmed-author:GuarneriCC	lld:pubmed
pubmed-article:16202223	pubmed:author	pubmed-author:GuarneriFF	lld:pubmed
pubmed-article:16202223	pubmed:issnType	Print	lld:pubmed
pubmed-article:16202223	pubmed:volume	9	lld:pubmed
pubmed-article:16202223	pubmed:owner	NLM	lld:pubmed
pubmed-article:16202223	pubmed:authorsComplete	Y	lld:pubmed
pubmed-article:16202223	pubmed:pagination	741-4	lld:pubmed
pubmed-article:16202223	pubmed:dateRevised	2011-11-17	lld:pubmed
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pubmed-article:16202223	pubmed:meshHeading	pubmed-meshheading:16202223...	lld:pubmed
pubmed-article:16202223	pubmed:articleTitle	Helicobacter pylori and autoimmune pancreatitis: role of carbonic anhydrase via molecular mimicry?	lld:pubmed
pubmed-article:16202223	pubmed:affiliation	Istituto di Dermatologia, Policlinico Gaetano Martino, Università di Messina, Messina, Italy. f.guarneri@tiscali.it	lld:pubmed
pubmed-article:16202223	pubmed:publicationType	Journal Article	lld:pubmed
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