File Download
  Links for fulltext
     (May Require Subscription)
Supplementary

Article: CD28-deficient mice are highly resistant to collagen-induced arthritis

TitleCD28-deficient mice are highly resistant to collagen-induced arthritis
Authors
Issue Date1999
Citation
Journal of Immunology, 1999, v. 162, n. 1, p. 203-208 How to Cite?
AbstractCD28 provides a critical costimulatory signal in Ag-specific T cell activation. Recent studies have revealed an important role for CD28 in the development of autoimmune diseases. We have examined the role of CD28 in collagen-induced arthritis (CIA) by inducing CIA in CD28-deficient DBA/1 mice. CD28-deficient mice never developed arthritis and showed markedly decreased levels of IgG and IgM anti-type II collagen (CII) Abs. In addition, the CD28(+/-) mice had similar levels of IgG1 and IgG2a anti-CII Abs, whereas in the CD28-deficient mice the level of IgG1 anti-CII Abs was decreased compared with that of IgG2a. IFN-γ production by lymph node cells in response to CII was also reduced. CD28-deficient mice were either immunized four times with CIII in CFA to augment Ag loading or given low doses of IL- 12 to enhance Th1 type responses. Both treatments resulted in a very low incidence of CIA development and minimal disease. CD28-deficient mice developed arthritis from injection of lymph node cells from CII-immunized wild-type mice, followed by immunization with CII in CFA. Taken together, these results indicate that costimulation of CD28 cannot be replaced by repeated activation through TCR or other costimulatory molecules. Thus, CD28 plays a critical role in both cellular and humoral immunity against CII and is indispensable for the development of CIA.
Persistent Identifierhttp://hdl.handle.net/10722/291480
ISSN
2023 Impact Factor: 3.6
2023 SCImago Journal Rankings: 1.558
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorTada, Yoshifumi-
dc.contributor.authorNagasawa, Kohei-
dc.contributor.authorHo, Alexandra-
dc.contributor.authorMorito, Fumiaki-
dc.contributor.authorUshiyama, Osamu-
dc.contributor.authorSuzuki, Noriaki-
dc.contributor.authorOhta, Hideaki-
dc.contributor.authorMak, Tak Wah-
dc.date.accessioned2020-11-17T14:54:27Z-
dc.date.available2020-11-17T14:54:27Z-
dc.date.issued1999-
dc.identifier.citationJournal of Immunology, 1999, v. 162, n. 1, p. 203-208-
dc.identifier.issn0022-1767-
dc.identifier.urihttp://hdl.handle.net/10722/291480-
dc.description.abstractCD28 provides a critical costimulatory signal in Ag-specific T cell activation. Recent studies have revealed an important role for CD28 in the development of autoimmune diseases. We have examined the role of CD28 in collagen-induced arthritis (CIA) by inducing CIA in CD28-deficient DBA/1 mice. CD28-deficient mice never developed arthritis and showed markedly decreased levels of IgG and IgM anti-type II collagen (CII) Abs. In addition, the CD28(+/-) mice had similar levels of IgG1 and IgG2a anti-CII Abs, whereas in the CD28-deficient mice the level of IgG1 anti-CII Abs was decreased compared with that of IgG2a. IFN-γ production by lymph node cells in response to CII was also reduced. CD28-deficient mice were either immunized four times with CIII in CFA to augment Ag loading or given low doses of IL- 12 to enhance Th1 type responses. Both treatments resulted in a very low incidence of CIA development and minimal disease. CD28-deficient mice developed arthritis from injection of lymph node cells from CII-immunized wild-type mice, followed by immunization with CII in CFA. Taken together, these results indicate that costimulation of CD28 cannot be replaced by repeated activation through TCR or other costimulatory molecules. Thus, CD28 plays a critical role in both cellular and humoral immunity against CII and is indispensable for the development of CIA.-
dc.languageeng-
dc.relation.ispartofJournal of Immunology-
dc.titleCD28-deficient mice are highly resistant to collagen-induced arthritis-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.pmid9886387-
dc.identifier.scopuseid_2-s2.0-0032963292-
dc.identifier.volume162-
dc.identifier.issue1-
dc.identifier.spage203-
dc.identifier.epage208-
dc.identifier.isiWOS:000077748100026-
dc.identifier.issnl0022-1767-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats