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Article: Resistance to activation-induced cell death and elevated FLIPL expression of CD4+ T cells in a polyI:C-induced primary biliary cirrhosis mouse model

TitleResistance to activation-induced cell death and elevated FLIPL expression of CD4+ T cells in a polyI:C-induced primary biliary cirrhosis mouse model
Authors
KeywordsSpecies Index: Animalia
Mus
Issue Date2009
PublisherSpringer-Verlag Italia Srl. The Journal's web site is located at http://www.springer.it/libri_libro.asp?id=238
Citation
Clinical and Experimental Medicine, 2009, v. 9 n. 4, p. 269-276 How to Cite?
AbstractPrimary biliary cirrhosis (PBC) is a type of organ-specific autoimmune disease in which immune tolerance is impaired by an unknown mechanism. We established a PBC animal model by injecting C57BL/6 mice with polyI:C to study activation-induced cell death (AICD) in CD4+ T lymphocytes and changes of apoptosis-associated molecules as a first step to understand the immune tolerance of PBC mice. Obvious inflammatory cell infiltration was observed in the portal area of the liver tissues in model mice and antimitochondrial antibodies (AMA) positive rate was 80%. The AICD level in both splenic and hepatic CD4+ T cells in the model group were all lower than those in controls, and in the model group the level for hepatic CD4+ T cells were significantly lower than that for splenic CD4+ T cells. Quantitative PCR revealed that FasL mRNA and TRAIL expression in CD4+ T cells in the model group decreased significantly compared with that in the control group. Western blots revealed that the expression of the anti-apoptotic protein FLIPL in the model group increased significantly with the FLIPL expression in hepatic CD4+ T cells significantly higher than that in splenic CD4+ T cells. There was a positive linear correlation between the number of infiltrated portal areas and relative expression of FLIPL in splenic CD4+ T cells in model group. There were no obvious changes for caspase-8 in either group. These results show that the anti-apoptotic ability of CD4+ T lymphocytes play an important role in immune tolerance in the PBC mouse model, and elevated FLIPL expression may enhance this ability. The inhibition of FasL and TRAIL expression may also help enhance this anti-apoptotic ability in CD4+ T lymphocytes and contribute to the aggravation of portal area inflammation. © 2009 Springer-Verlag.
Persistent Identifierhttp://hdl.handle.net/10722/92190
ISSN
2015 Impact Factor: 2.854
2015 SCImago Journal Rankings: 0.849
ISI Accession Number ID
Funding AgencyGrant Number
National High- tech R& D Program (863 Program)2006AA02Z496
funds for Excellent Department Leader, Science and Technology Commission of Shanghai Municipality07XD14013
Funding Information:

We thank Dr. Hongyu Yu and Lingzhen Zhang for technical assistance. This research was supported by National High- tech R& D Program (863 Program), code no.: 2006AA02Z496, Subject: Early diagnosis and immune tolerance reconstruction of autoimmune diseases; and funds for Excellent Department Leader, Science and Technology Commission of Shanghai Municipality, code no.: 07XD14013, Subject: The role of Toll- like receptors in primary biliary cirrhosis and atherosclerosis.

References

 

DC FieldValueLanguage
dc.contributor.authorJiang, Ten_HK
dc.contributor.authorHan, Zen_HK
dc.contributor.authorChen, Sen_HK
dc.contributor.authorWu, Cen_HK
dc.contributor.authorTang, Yen_HK
dc.contributor.authorQian, Cen_HK
dc.contributor.authorChen, Yen_HK
dc.contributor.authorZhou, Yen_HK
dc.contributor.authorZhu, Yen_HK
dc.contributor.authorGu, Men_HK
dc.contributor.authorZhu, Len_HK
dc.contributor.authorYao, Den_HK
dc.contributor.authorDeng, Aen_HK
dc.contributor.authorZhong, Ren_HK
dc.date.accessioned2010-09-17T10:38:44Z-
dc.date.available2010-09-17T10:38:44Z-
dc.date.issued2009en_HK
dc.identifier.citationClinical and Experimental Medicine, 2009, v. 9 n. 4, p. 269-276en_HK
dc.identifier.issn1591-8890en_HK
dc.identifier.urihttp://hdl.handle.net/10722/92190-
dc.description.abstractPrimary biliary cirrhosis (PBC) is a type of organ-specific autoimmune disease in which immune tolerance is impaired by an unknown mechanism. We established a PBC animal model by injecting C57BL/6 mice with polyI:C to study activation-induced cell death (AICD) in CD4+ T lymphocytes and changes of apoptosis-associated molecules as a first step to understand the immune tolerance of PBC mice. Obvious inflammatory cell infiltration was observed in the portal area of the liver tissues in model mice and antimitochondrial antibodies (AMA) positive rate was 80%. The AICD level in both splenic and hepatic CD4+ T cells in the model group were all lower than those in controls, and in the model group the level for hepatic CD4+ T cells were significantly lower than that for splenic CD4+ T cells. Quantitative PCR revealed that FasL mRNA and TRAIL expression in CD4+ T cells in the model group decreased significantly compared with that in the control group. Western blots revealed that the expression of the anti-apoptotic protein FLIPL in the model group increased significantly with the FLIPL expression in hepatic CD4+ T cells significantly higher than that in splenic CD4+ T cells. There was a positive linear correlation between the number of infiltrated portal areas and relative expression of FLIPL in splenic CD4+ T cells in model group. There were no obvious changes for caspase-8 in either group. These results show that the anti-apoptotic ability of CD4+ T lymphocytes play an important role in immune tolerance in the PBC mouse model, and elevated FLIPL expression may enhance this ability. The inhibition of FasL and TRAIL expression may also help enhance this anti-apoptotic ability in CD4+ T lymphocytes and contribute to the aggravation of portal area inflammation. © 2009 Springer-Verlag.en_HK
dc.languageengen_HK
dc.publisherSpringer-Verlag Italia Srl. The Journal's web site is located at http://www.springer.it/libri_libro.asp?id=238en_HK
dc.relation.ispartofClinical and Experimental Medicineen_HK
dc.subjectSpecies Index: Animaliaen_HK
dc.subjectMusen_HK
dc.titleResistance to activation-induced cell death and elevated FLIPL expression of CD4+ T cells in a polyI:C-induced primary biliary cirrhosis mouse modelen_HK
dc.typeArticleen_HK
dc.identifier.emailChen, Y:ychenc@hkucc.hku.hken_HK
dc.identifier.authorityChen, Y=rp1318en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1007/s10238-009-0052-2en_HK
dc.identifier.pmid19418018-
dc.identifier.scopuseid_2-s2.0-70349906268en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-70349906268&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume9en_HK
dc.identifier.issue4en_HK
dc.identifier.spage269en_HK
dc.identifier.epage276en_HK
dc.identifier.isiWOS:000270648500004-
dc.identifier.citeulike4495725-

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