Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2004-9-10
pubmed:abstractText
Collagen-induced arthritis (CIA) is a rodent model of human rheumatoid arthritis. Mice of the H-2(q) (DBA/1J) background are highly susceptible to disease whereas mice of the H-2(b) (C57BL/6, B6) background are resistant. To determine why B6 mice are resistant to disease induction, we systematically analyzed T and B cell immune responses in B6 mice, compared to DBA/1J mice, following immunization with bovine type II collagen (CII). We found that both strains showed similar T cell proliferation and cytokine responses and similar levels of anti-CII antibodies (Abs) at day 12 or day 14 of initial immunization (primary immune response), however, those B6 mice that did not develop arthritis showed a significant defect in T cell responses and significantly lower levels of anti-CII Abs following secondary boosting immunization (day 35 of initial immunization, secondary immune response) compared to DBA/1J mice. Our results define for the first time that a defective secondary immune responses in B6 mice leads to the resistance of CIA.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0271-9142
pubmed:author
pubmed:issnType
Print
pubmed:volume
24
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
481-91
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
Resistance to development of collagen-induced arthritis in C57BL/6 mice is due to a defect in secondary, but not in primary, immune response.
pubmed:affiliation
Section of Rheumatology, Yale School of Medicine, New Haven, Connecticut 06520-8031, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't