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Background Interleukin 1 (IL-1) is a major contributor to the development of immune-mediated arthritis. BALB/c mice that are homozygous for the deficiency (BALB/c) spontaneously develop joint-specific inflammation that resembles human rheumatoid arthritis [1]. To understand the role of genetic factors involved in the development of spontaneous arthritis (SAD) in mice deficient in IL-1 receptor antagonist protein (IL_1RA), we have identified a genomic region containing a major quantitative trait locus (QTL) for this disease. The QTL is on chromosome 1 and appears to be the strongest genetic region regulating arthritis [2]. To confirm the importance of this QTL in SAD, we next developed congenic mouse strains that contain the strong QTL genomic fragments from BALB/c on a DBA/1 genetic background [3] and conversely a similar genomic fragment from DBA/1 on a BALB/c background. When the DBA/1 fragment was placed on a BALB/c background, arthritis was delayed and less severe. When the BALB/c fragment was placed on a DBA/1 background, arthritis occurred in varying degrees.

Analysis of effect of congenic mice on the gene expression under genomic background of BALB/c mice