| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Department of Immunology, The Scripps Research Institute, La Jolla, CA 92037
F1 hybrids among New Zealand Black (NZB), New Zealand White (NZW), and BXSB lupus-prone strains develop accelerated autoimmunity in both sexes regardless of the specific combination. To identify BXSB susceptibility loci in the absence of the Y chromosome accelerator of autoimmunity (Yaa) and to study the genetics of this complementation, genome-wide quantitative trait locus (QTL) mapping was performed on female (BXSB x NZW)F2 mice. Six QTL were identified on chromosomes 1, 4, 5, 6, 7, and 17. Survival mapped to chromosomes 5 and 17, anti-chromatin Ab to chromosomes 4 and 17, glomerulonephritis to chromosomes 6 and 17, and splenomegaly to chromosomes 1, 7, and 17. QTL on chromosomes 4 and 6 were new and designated as Lxw1 and -2, respectively. Two non-MHC QTL (chromosomes 1 and 4) were inherited from the BXSB and the rest were NZW-derived, including two similar to previously defined loci. Only two of 11 previously defined non-MHC BXSB QTL using male (Yaa+) crosses were implicated, suggesting that some male-defined BXSB QTL may require coexpression of the Yaa. Findings from this and other studies indicate that BXSB and NZB backgrounds contribute completely different sets of genes to complement NZW mice. Identification of susceptibility genes and complementing genes in several lupus-prone strain combinations will be important for defining the epistatic effects and background influences on the heterogeneous genetic factors responsible for lupus induction.
This article has been cited by other articles:
|
|
 |
|
  Y. Hamano, K. Tsukamoto, M. Abe, G. D. Sun, D. Zhang, H. Fujii, S. Matsuoka, M. Tanaka, A. Ishida-Okawara, H. Tachikawa, et al. Genetic Dissection of Vasculitis, Myeloperoxidase-Specific Antineutrophil Cytoplasmic Autoantibody Production, and Related Traits in Spontaneous Crescentic Glomerulonephritis-Forming/Kinjoh Mice J. Immunol., March 15, 2006; 176(6): 3662 - 3673. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Wakui, L. Morel, E. J. Butfiloski, C. Kim, and E. S. Sobel Genetic Dissection of Systemic Lupus Erythematosus Pathogenesis: Partial Functional Complementation between Sle1 and Sle3/5 Demonstrates Requirement for Intracellular Coexpression for Full Phenotypic Expression of Lupus J. Immunol., July 15, 2005; 175(2): 1337 - 1345. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. E. K. Haywood, N. J. Rogers, S. J. Rose, J. Boyle, A. McDermott, J. M. Rankin, V. Thiruudaian, M. R. Lewis, L. Fossati-Jimack, S. Izui, et al. Dissection of BXSB Lupus Phenotype Using Mice Congenic for Chromosome 1 Demonstrates That Separate Intervals Direct Different Aspects of Disease J. Immunol., October 1, 2004; 173(7): 4277 - 4285. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
