Linked Life Data

19239928

Source:http://linkedlifedata.com/resource/pubmed/id/19239928

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2009-5-18
pubmed:abstractText
Viral infections are most likely triggering factors of autoimmune diseases, although a single vial infection is not sufficient to cause clinically evident autoimmune diseases. Any disease that profoundly alters the immune system may cause perturbed viral infections, thereby rendering otherwise refractory patients susceptible to autoimmune diseases. In this regard, drug-induced hypersensitivity syndrome (DIHS), a drug rash characterized by sequential reactivations of herpesviruses and the subsequent development of autoimmune diseases, offers a unique opportunity to investigate the mechanism of how autoimmunity is elicited after viral infections. Indeed, several autoimmune diseases have been reported to occur at intervals of several months to years after clinical resolution of DIHS. Two representative cases who developed autoimmune diseases three to four years after DIHS are shown. Our recent analyses of the kinetics of a developing disease have shown that fully functional FoxP3(+) regulatory T (Treg) cells are expanded at the acute stage thereby allowing viral reactivations but lose their suppressive function coincident with their contraction upon clinical resolution. The functional defect of Treg cells would be responsible for the subsequent development of autoimmune diseases. Patients with DIHS need close monitoring because of possible progression to autoimmune diseases even after the complete resolution.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1873-0183
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
8
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
488-94
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Viral connection between drug rashes and autoimmune diseases: how autoimmune responses are generated after resolution of drug rashes.
pubmed:affiliation
Department of Dermatology, Kyorin University School of Medicine, Mitaka, Tokyo, Japan. nrkcc0605-ao@ks.kyorin-u.ac.jp
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't