Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
1994-5-5
pubmed:databankReference
pubmed:abstractText
Type II collagen-induced arthritis (CIA) in mice is an animal model of autoimmune inflammatory arthritis. Arthritis is induced in susceptible strains of mice (H-2q and H-2r) after immunization with heterologous or autologous type II collagen in CFA. Induction of CIA is T cell dependent and a restricted usage of TCR V beta genes has been found in the arthritic joints and lymph nodes of mice with CIA. However, genes within the MHC are not the only determinants of susceptibility to CIA as SWR/j, AU/ssJ (both H-2q) and RIIIS/J(H-2r) mice are resistant to the induction of CIA. These strains of mice are TCR V beta chain genes deletion mutants (TCR V beta a and TCR V beta c haplotypes) and it was hypothesized that these mice are resistant to CIA because of the absence of a particular set of V beta TCR genes that are genomically deleted in these strains of mice. We now show that BUB/BnJ mice (H-2q) are T cell subsets deficient because of the genomic deletion of TCR V beta 5, 8, 9, 11, 12, and 13 sub-families. Our data demonstrate that despite the deficiency in T cell subsets from genomic deletion of TCR V beta genes, BUB mice are highly susceptible to the development of CIA. These results indicate that genomic deletion of certain TCR V beta genes alone is not in itself sufficient to confer resistance to CIA. These results further suggest that other unknown gene(s) must also contribute to the induction of CIA.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
152
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4175-82
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
BUB/BnJ (H-2q) is a TCR deletion mutant mouse strain (TCR V beta a, KJ16-) that is susceptible to type II collagen-induced arthritis.
pubmed:affiliation
Department of Medicine, Case Western Reserve University School of Medicine, Cleveland, OH 44106.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.