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dc.contributor.authorSajadi, Seyyed Mohammad Ali
dc.contributor.authorMirzaei, Vahid
dc.contributor.authorHassanshahi, Gholamhossein
dc.contributor.authorKhorramdelazad, Hossein
dc.contributor.authorDaredor, Hassan Yousefi
dc.contributor.authorHosseini, Seyyed Mohammad Hossein
dc.contributor.authorMoogooi, Mojgan
dc.contributor.authorRavary, Ali
dc.contributor.authorArababadi, Mohammad Kazemi
dc.contributor.authorKennedy, Derek
dc.date.accessioned2018-03-26T01:30:47Z
dc.date.available2018-03-26T01:30:47Z
dc.date.issued2013
dc.date.modified2014-01-31T04:43:53Z
dc.identifier.issn0003-9985
dc.identifier.doi10.5858/arpa.2012-0415-OA
dc.identifier.urihttp://hdl.handle.net/10072/56339
dc.description.abstractContext.-Toll-like receptors (TLRs) play crucial roles in immune responses, especially innate immunity, against viral infections. Toll-like receptor 9 recognizes intracellular viral double-strand DNA, which leads to the activation of nuclear factor B (NF-jB) through the myeloid differentiation primary response 88 (MYD88) pathway. Defects in the expression of TLR9 and its signaling molecules may cause attenuated immune responses against hepatitis B virus. Objective.-To determine expression levels of TLR9 messenger RNA along with MYD88, interleukin 1 receptor-associated kinase 1 (IRAK1), tumor necrosis factor receptor-associated factor 6 (TRAF6), and NF-jB in the peripheral blood mononuclear cells obtained from chronic hepatitis B virus (CHB)-infected patients. Design.-In this study, 60 CHB patients and 60 healthy controls were recruited and the expression of TLR9 and its downstream signaling molecules was examined by realtime polymerase chain reaction techniques using b-actin as a housekeeping gene. Results.-Our results showed that expression of TLR9, MYD88, IRAK1, TRAF6, and NF-jB in peripheral blood mononuclear cells of CHB patients was significantly decreased in comparison with healthy controls. Conclusions.-According to our results, it appears that CHB patients are unable to appropriately express genes in the TLR9 pathway, which may impede immune responses against hepatitis B virus infection. These results suggest a mechanism that may partially explain the fact that immune responses are disrupted in CHB patients
dc.description.peerreviewedYes
dc.description.publicationstatusYes
dc.languageEnglish
dc.publisherCollege of American Pathologists
dc.publisher.placeUnited States
dc.relation.ispartofstudentpublicationN
dc.relation.ispartofpagefrom1674
dc.relation.ispartofpageto1679
dc.relation.ispartofjournalArchives of Pathology & Laboratory Medicine
dc.relation.ispartofvolume137
dc.rights.retentionY
dc.subject.fieldofresearchMedical Virology
dc.subject.fieldofresearchClinical Sciences
dc.subject.fieldofresearchcode110804
dc.subject.fieldofresearchcode1103
dc.titleDecreased Expressions of Toll-Like Receptor 9 and Its Signaling Molecules in Chronic Hepatitis B Virus-Infected Patients
dc.typeJournal article
dc.type.descriptionC1 - Articles
dc.type.codeC - Journal Articles
gro.date.issued2013
gro.hasfulltextNo Full Text
gro.griffith.authorKennedy, Derek D.


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