File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: CD44-Deficient mice exhibit enhanced hepatitis after concanavalin A injection: Evidence for involvement of CD44 in activation-induced cell death

TitleCD44-Deficient mice exhibit enhanced hepatitis after concanavalin A injection: Evidence for involvement of CD44 in activation-induced cell death
Authors
Issue Date2001
Citation
Journal of Immunology, 2001, v. 166, n. 10, p. 5889-5897 How to Cite?
AbstractAdministration of Con A induces severe injury to hepatocytes in mice and is considered to be a model for human hepatitis. In the current study, we investigated the role of CD44 in Con A-induced hepatitis. Intravenous administration of Con A (20 mg/kg) caused 100% mortality in C57BL/6 CD44-knockout (KO) mice, although it was not lethal in C57BL/6 CD44 wild-type (WT) mice. Administration of lower doses of Con A (12 mg/kg body weight) into CD44 WT mice induced hepatitis as evident from increased plasma aspartate aminotransferase levels accompanied by active infiltration of mononuclear cells and neutrophils, and significant induction of apoptosis in the liver. Interestingly, CD44 KO mice injected with similar doses of Con A exhibited more severe acute suppurative hepatitis. Transfer of spleen cells from Con A-injected CD44 KO mice into CD44 WT mice induced higher levels of hepatitis when compared with transfer of similar cells from CD44 WT mice into CD44 WT mice. The increased hepatitis seen in CD44 KO mice was accompanied by increased production of cytokines such as TNF-α, IL-2 and IFN-γ, but not Fas or Fas ligand. The increased susceptibility of CD44 KO mice to hepatitis correlated with the observation that T cells from CD44 KO mice were more resistant to activation-induced cell death when compared with the CD44 WT mice. Together, these data demonstrate that activated T cells use CD44 to undergo apoptosis, and dysregulation in this pathway could lead to increased pathogenesis in a number of diseases, including hepatitis.
Persistent Identifierhttp://hdl.handle.net/10722/291585
ISSN
2021 Impact Factor: 5.426
2020 SCImago Journal Rankings: 2.737
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorChen, Dawei-
dc.contributor.authorMcKallip, Robert J.-
dc.contributor.authorZeytun, Ahmet-
dc.contributor.authorDo, Yoonkyung-
dc.contributor.authorLombard, Catherine-
dc.contributor.authorRobertson, John L.-
dc.contributor.authorMak, Tak W.-
dc.contributor.authorNagarkatti, Prakash S.-
dc.contributor.authorNagarkatti, Mitzi-
dc.date.accessioned2020-11-17T14:54:41Z-
dc.date.available2020-11-17T14:54:41Z-
dc.date.issued2001-
dc.identifier.citationJournal of Immunology, 2001, v. 166, n. 10, p. 5889-5897-
dc.identifier.issn0022-1767-
dc.identifier.urihttp://hdl.handle.net/10722/291585-
dc.description.abstractAdministration of Con A induces severe injury to hepatocytes in mice and is considered to be a model for human hepatitis. In the current study, we investigated the role of CD44 in Con A-induced hepatitis. Intravenous administration of Con A (20 mg/kg) caused 100% mortality in C57BL/6 CD44-knockout (KO) mice, although it was not lethal in C57BL/6 CD44 wild-type (WT) mice. Administration of lower doses of Con A (12 mg/kg body weight) into CD44 WT mice induced hepatitis as evident from increased plasma aspartate aminotransferase levels accompanied by active infiltration of mononuclear cells and neutrophils, and significant induction of apoptosis in the liver. Interestingly, CD44 KO mice injected with similar doses of Con A exhibited more severe acute suppurative hepatitis. Transfer of spleen cells from Con A-injected CD44 KO mice into CD44 WT mice induced higher levels of hepatitis when compared with transfer of similar cells from CD44 WT mice into CD44 WT mice. The increased hepatitis seen in CD44 KO mice was accompanied by increased production of cytokines such as TNF-α, IL-2 and IFN-γ, but not Fas or Fas ligand. The increased susceptibility of CD44 KO mice to hepatitis correlated with the observation that T cells from CD44 KO mice were more resistant to activation-induced cell death when compared with the CD44 WT mice. Together, these data demonstrate that activated T cells use CD44 to undergo apoptosis, and dysregulation in this pathway could lead to increased pathogenesis in a number of diseases, including hepatitis.-
dc.languageeng-
dc.relation.ispartofJournal of Immunology-
dc.titleCD44-Deficient mice exhibit enhanced hepatitis after concanavalin A injection: Evidence for involvement of CD44 in activation-induced cell death-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.4049/jimmunol.166.10.5889-
dc.identifier.pmid11342603-
dc.identifier.scopuseid_2-s2.0-0035873417-
dc.identifier.volume166-
dc.identifier.issue10-
dc.identifier.spage5889-
dc.identifier.epage5897-
dc.identifier.isiWOS:000170948500007-
dc.identifier.issnl0022-1767-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats