Email updates

Keep up to date with the latest news and content from BMC Bioinformatics and BioMed Central.

This article is part of the supplement: UT-ORNL-KBRIN Bioinformatics Summit 2008

Open Access Poster presentation

QTL mapping arthritis traits in CXB mice

Dana Marshall1*, Jeremy Peirce23, Fang Zhou4, Lu Lu3, Rob Williams3, Ken Manly3 and John Stuart45

Author Affiliations

1 Department of Surgery, Meharry Medical College, Nashville, TN 37208, USA

2 Illumina Inc., San Diego, CA, 92121, USA

3 Department of Neuroscience, University of Tennessee Health Science Center, Memphis, TN 38104, USA

4 Department of Rheumatology, University of Tennessee Health Science Center, Memphis, TN 38104, USA

5 Research Division, Veterans Affairs Medical Center, Memphis, TN 38104, USA

For all author emails, please log on.

BMC Bioinformatics 2008, 9(Suppl 7):P10  doi:10.1186/1471-2105-9-S7-P10

The electronic version of this article is the complete one and can be found online at: http://www.biomedcentral.com/1471-2105/9/S7/P10


Published:8 July 2008

© 2008 Marshall et al; licensee BioMed Central Ltd.

Poster presentation

B6 mice are of intermediate susceptibility to collagen-induced arthritis (CIA) while Balb/c mice are resistant, but are highly susceptible to proteoglycan-induced arthritis. Antigen presentation is H-2 directed but the disease that results is thought to be driven by regions outside of the MHC therefore, CXB mouse strains afford the opportunity to look at the influence of these regions on CIA. H2-b CXB strains are predicted to show variation in disease parameters relative to C57Bl/6, depending on which Balb/c chromosome regions is present. Nine of thirteen CXB strains are H-2b while one has a recombined H-2 region (CXB9). The four H-2d strains were crossed with C57Bl/6ByJ to generate F1 mice that could present collagen via the B6-contributed H-2b locus, while possibly identifying Balb/c loci that would have a dominant effect on disease progression. A number of disease and immunological parameters were collected and gene expression analysis was done on resting spleens. A range of incidence and severity of disease was seen and mice were assigned to susceptibility groups based on collected parameters. Preliminary QTL analysis has identified regions on chromosomes 13, 15 and 19 that correlate with susceptibility to CIA.