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Sle2  -  systemic lupus erythmatosus susceptibility 2

Mus musculus

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Disease relevance of Sle2


High impact information on Sle2

  • Sle1 mediates the loss of tolerance to nuclear antigens; Sle2 lowers the activation threshold of B cells; and Sle3 mediates a dysregulation of CD4(+) T cells [1].
  • The combination of Sle1 with Sle2, Sle3, or the BXSB-derived autoimmune accelerating gene yaa results in the development of systemic autoimmunity with variably penetrant severe glomerulonephritis culminating in kidney failure [1].
  • These results show that the Sle2 locus contains several loci affecting B cell development, with only the two NZW-derived loci having the least effect of B-1a cell accumulation significantly contributing to lupus pathogenesis [2].
  • Given that the locus for IFN-I is positioned within the Sle2 murine lupus susceptibility interval on chromosome 4, we undertook this study to investigate whether differences in IFN-I levels might potentially contribute to the phenotypes ascribed to this locus [4].
  • CONCLUSION: Unexpectedly, reduction of IFN-I levels reproduced the serologic and cellular phenotypes previously associated with the Sle2 lupus susceptibility interval [4].

Biological context of Sle2

  • In this paper, we examined the mechanisms responsible for this phenotype by comparing congenic C57BL/6 mice with or without Sle2 [5].
  • Sle2 on chromosome 4 was significantly linked to glomerulonephritis in a linkage analysis of a NZM2410 x B6 cross [2].
  • Increased proliferation and decreased apoptosis did not affect Sle2 peritoneal B-2 cells [5].

Anatomical context of Sle2

  • Yet, Sle2 expression alone on a C57BL/6 background did not result in any clinical manifestation, but in an abnormal B cell development, including the accumulation of B-1a cells in the peritoneal cavity and spleen [2].
  • In addition, a significant number of peritoneal cavity B-1a cells were recovered in lethally irradiated B6.Sle2 mice reconstituted with B6.Igh(a) bone marrow, showing radiation resistance in Sle2 B-1a cells or its precursors [5].
  • The focus of this study was to understand how Sle2 on murine chromosome 4 impacts the immune system [3].

Other interactions of Sle2

  • In contrast, two locus combinations of Sle2, Sle3, and yaa failed to mediate fatal disease [1].

Analytical, diagnostic and therapeutic context of Sle2


  1. Genetic reconstitution of systemic lupus erythematosus immunopathology with polycongenic murine strains. Morel, L., Croker, B.P., Blenman, K.R., Mohan, C., Huang, G., Gilkeson, G., Wakeland, E.K. Proc. Natl. Acad. Sci. U.S.A. (2000) [Pubmed]
  2. Genetic dissection of the murine lupus susceptibility locus Sle2: contributions to increased peritoneal B-1a cells and lupus nephritis map to different loci. Xu, Z., Duan, B., Croker, B.P., Wakeland, E.K., Morel, L. J. Immunol. (2005) [Pubmed]
  3. Genetic dissection of systemic lupus erythematosus pathogenesis: Sle2 on murine chromosome 4 leads to B cell hyperactivity. Mohan, C., Morel, L., Yang, P., Wakeland, E.K. J. Immunol. (1997) [Pubmed]
  4. Deficiency of type I interferon contributes to Sle2-associated component lupus phenotypes. Li, J., Liu, Y., Xie, C., Zhu, J., Kreska, D., Morel, L., Mohan, C. Arthritis Rheum. (2005) [Pubmed]
  5. Mechanisms of peritoneal B-1a cells accumulation induced by murine lupus susceptibility locus Sle2. Xu, Z., Butfiloski, E.J., Sobel, E.S., Morel, L. J. Immunol. (2004) [Pubmed]
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