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Sle1  -  systemic lupus erythmatosus susceptibility 1

Mus musculus

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Disease relevance of Sle1


High impact information on Sle1


Biological context of Sle1

  • Genetic dissection of SLE pathogenesis. Sle1 on murine chromosome 1 leads to a selective loss of tolerance to H2A/H2B/DNA subnucleosomes [8].
  • These findings indicate that the potent autoimmune phenotype caused by the Sle1 genomic interval reflects the combined impact of four, separate, susceptibility genes [9].
  • OBJECTIVE: To assess the effects of altered class II major histocompatibility complex (MHCII) expression on circulating autoantibody levels in C57BL/6 (B6) mice congenic for the Sle1 (B6.Sle1 mice) or Nba2 (B6.Nba2 mice) regions [10].
  • B6.yaa mice are not overtly autoimmune, but the addition of Sle1, which contains the autoimmune-predisposing Slam/Cd2 haplotype, causes the development of fatal lupus with numerous immunological aberrations [11].
  • These experiments showed that Sle1 expression results in both B and T cells intrinsic defects and demonstrate that the documented involvement of each cell compartment in the production of anti-chromatin Abs corresponds to genetic defects rather than bystander effects [12].

Anatomical context of Sle1


Regulatory relationships of Sle1


Other interactions of Sle1

  • This suggests a major role for the FAS pathway in keeping in check the loss of tolerance mediated by the Sle1 loci, especially for Sle1a [4].
  • One of them (Cgnz1) is on the telomeric end of chromosome 1 and close to Sle1 [15].
  • We have used congenic strains to analyze the interactions between the Sle1 subloci and other lupus susceptibility loci using Y autoimmunity accelerator (Yaa) and Faslpr as sensitizing mutations [4].
  • Despite this suppression of the Sle1-mediated cell surface activation phenotypes, B6.Sle1 Sles1 splenic B cells still exhibit intrinsic ERK phosphorylation [16].
  • RESULTS: Two recessive susceptibility loci of the MRL allele were identified on chromosomes 4 and 1, which had previously been defined as the autoimmune related loci termed Arvm1 and Sle-1/Nba2, respectively [17].

Analytical, diagnostic and therapeutic context of Sle1


  1. Several genes contribute to the production of autoreactive B and T cells in the murine lupus susceptibility locus Sle1c. Chen, Y., Perry, D., Boackle, S.A., Sobel, E.S., Molina, H., Croker, B.P., Morel, L. J. Immunol. (2005) [Pubmed]
  2. Epistatic modifiers of autoimmunity in a murine model of lupus nephritis. Morel, L., Tian, X.H., Croker, B.P., Wakeland, E.K. Immunity (1999) [Pubmed]
  3. 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]
  4. Genetic interactions between susceptibility loci reveal epistatic pathogenic networks in murine lupus. Croker, B.P., Gilkeson, G., Morel, L. Genes Immun. (2003) [Pubmed]
  5. Identification and molecular characterization of an N-acetylmuramyl-L-alanine amidase Sle1 involved in cell separation of Staphylococcus aureus. Kajimura, J., Fujiwara, T., Yamada, S., Suzawa, Y., Nishida, T., Oyamada, Y., Hayashi, I., Yamagishi, J., Komatsuzawa, H., Sugai, M. Mol. Microbiol. (2005) [Pubmed]
  6. Cr2, a candidate gene in the murine Sle1c lupus susceptibility locus, encodes a dysfunctional protein. Boackle, S.A., Holers, V.M., Chen, X., Szakonyi, G., Karp, D.R., Wakeland, E.K., Morel, L. Immunity (2001) [Pubmed]
  7. Genetic dissection of SLE: SLE1 and FAS impact alternate pathways leading to lymphoproliferative autoimmunity. Shi, X., Xie, C., Kreska, D., Richardson, J.A., Mohan, C. J. Exp. Med. (2002) [Pubmed]
  8. Genetic dissection of SLE pathogenesis. Sle1 on murine chromosome 1 leads to a selective loss of tolerance to H2A/H2B/DNA subnucleosomes. Mohan, C., Alas, E., Morel, L., Yang, P., Wakeland, E.K. J. Clin. Invest. (1998) [Pubmed]
  9. The major murine systemic lupus erythematosus susceptibility locus, Sle1, is a cluster of functionally related genes. Morel, L., Blenman, K.R., Croker, B.P., Wakeland, E.K. Proc. Natl. Acad. Sci. U.S.A. (2001) [Pubmed]
  10. Dichotomous effects of complete versus partial class II major histocompatibility complex deficiency on circulating autoantibody levels in autoimmune-prone mice. Stohl, W., Xu, D., Metzger, T.E., Kim, K.S., Morel, L., Kotzin, B.L. Arthritis Rheum. (2004) [Pubmed]
  11. A Tlr7 translocation accelerates systemic autoimmunity in murine lupus. Subramanian, S., Tus, K., Li, Q.Z., Wang, A., Tian, X.H., Zhou, J., Liang, C., Bartov, G., McDaniel, L.D., Zhou, X.J., Schultz, R.A., Wakeland, E.K. Proc. Natl. Acad. Sci. U.S.A. (2006) [Pubmed]
  12. The major murine systemic lupus erythematosus susceptibility locus Sle1 results in abnormal functions of both B and T cells. Sobel, E.S., Satoh, M., Chen, Y., Wakeland, E.K., Morel, L. J. Immunol. (2002) [Pubmed]
  13. IL-6 Produced by Dendritic Cells from Lupus-Prone Mice Inhibits CD4+CD25+ T Cell Regulatory Functions. Wan, S., Xia, C., Morel, L. J. Immunol. (2007) [Pubmed]
  14. Genetic determination of T cell help in loss of tolerance to nuclear antigens. Chen, Y., Cuda, C., Morel, L. J. Immunol. (2005) [Pubmed]
  15. NZM2328: a new mouse model of systemic lupus erythematosus with unique genetic susceptibility loci. Waters, S.T., Fu, S.M., Gaskin, F., Deshmukh, U.S., Sung, S.S., Kannapell, C.C., Tung, K.S., McEwen, S.B., McDuffie, M. Clin. Immunol. (2001) [Pubmed]
  16. Epistatic suppression of systemic lupus erythematosus: fine mapping of Sles1 to less than 1 mb. Subramanian, S., Yim, Y.S., Liu, K., Tus, K., Zhou, X.J., Wakeland, E.K. J. Immunol. (2005) [Pubmed]
  17. An epistatic effect of the female specific loci on the development of autoimmune vasculitis and antinuclear autoantibody in murine lupus. Zhang, M.C., Misu, N., Furukawa, H., Watanabe, Y., Terada, M., Komori, H., Miyazaki, T., Nose, M., Ono, M. Ann. Rheum. Dis. (2006) [Pubmed]
  18. Genetic dissection of SLE pathogenesis: adoptive transfer of Sle1 mediates the loss of tolerance by bone marrow-derived B cells. Sobel, E.S., Mohan, C., Morel, L., Schiffenbauer, J., Wakeland, E.K. J. Immunol. (1999) [Pubmed]
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