157
Views
8
CrossRef citations to date
0
Altmetric
Research Papers

Regulation of basement membrane-reactive B cells in BXSB, (NZBxNZW)F1, NZB, and MRL/lpr lupus mice

, , , , , & show all
Pages 188-204 | Received 10 May 2012, Accepted 31 Oct 2012, Published online: 09 Jan 2013

References

  • Harley I. T., Kaufman K. M., Langefeld C. D., Harley J. B., Kelly J. A.. Genetic susceptibility to SLE: New insights from fine mapping and genome-wide association studies. Nat. Rev. Genetics. 2009; 10 5: 285–290.
  • Ramos P. S., Brown E. E., Kimberly R. P., Langefeld C. D.. Genetic factors predisposing to systemic lupus erythematosus and lupus nephritis. Semin. Nephrol.. 2010; 30 2: 164–176.
  • Kono D. H., Theofilopoulos A. N.. Genetics of SLE in mice. Springer Semin. Immunopathol.. 2006; 28 2: 83–96.
  • Morel L.. Genetics of SLE: evidence from mouse models. Nat. Rev. Rheumatol.. 2010; 6:348–357.
  • Pathak S., Mohan C.. Cellular and molecular pathogenesis of systemic lupus erythematosus: lessons from animal models. Arthritis Res. Ther.. 2011; 13 5: 241.
  • Kyogoku C., Langefeld C. D., Ortmann W. A., . Genetic association of the R620W polymorphism of protein tyrosine phosphatase PTPN22 with human SLE. Am. J. Hum. Genet.. 2004; 75 3: 504–507.
  • Kozyrev S. V., Abelson A. K., Wojcik J., . Functional variants in the B-cell gene BANK1 are associated with systemic lupus erythematosus. Nat. Genet.. 2008; 40 2: 211–216.
  • Cunninghame Graham D. S., Graham R. R., Manku H., . Polymorphism at the TNF superfamily gene TNFSF4 confers susceptibility to systemic lupus erythematosus. Nat. Genet.. 2008; 40 1: 83–89.
  • Gateva V., Sandling J. K., Hom G., . A large-scale replication study identifies TNIP1, PRDM1, JAZF1, UHRF1BP1 and IL10 as risk loci for systemic lupus erythematosus. Nat. Genet.. 2009; 41 11: 1228–1233.
  • Cunninghame Graham D. S., Morris D. L., Bhangale T. R., . Association of NCF2, IKZF1, IRF8, IFIH1, and TYK2 with systemic lupus erythematosus. PLoS Genet.. 2011; 7 10: e1002341.
  • Zhou X. J., Lu X. L., Nath S. K., . Gene-gene interaction of BLK, TNFSF4, TRAF1, TNFAIP3, and REL in systemic lupus erythematosus. Arthritis Rheum.. 2012; 64 1: 222–231.
  • Chung S. A., Taylor K. E., Graham R. R., . Differential genetic associations for systemic lupus erythematosus based on anti-dsDNA autoantibody production. PLoS Genet.. 2011; 7 3: e1001323 Epub 2011/03/17.
  • Hall S. W., Cooke A.. Autoimmunity and inflammation: murine models and translational studies. Mammal. Genome J. Inter. Mammal. Genome Soc.. 2011; 22 7–8: 377–389 Epub 2011/06/19. doi: 10.1007/s00335-011-9338-2.
  • Sabbaga J., Line S. R. P., Potocnjak P., Madaio M. P.. A murine nephritogenic monoclonal anti-DNA autoantibody binds directly to mouse laminin, the major non-collagenous protein component of the glomerular basement membrane. Eur. J. Immunol.. 1989; 19:137–143.
  • Foster M. H., Sabbaga J., Line S. R. P., . Molecular analysis of nephrotropic anti-laminin antibodies from an MRL/lpr autoimmune mouse. J. Immunol.. 1993; 151:814–824.
  • Ben-Yehuda A., Rasooly L., Bar-Tana R., . The urine of SLE patients contains antibodies that bind to the laminin component of the extracellular matrix. J. Autoimmun.. 1995; 8:279–291.
  • Amital H., Heilweil M., Ulmansky R., . Treatment with a laminin-derived peptide suppresses lupus nephritis. J. Immunol.. 2005; 175 8: 5516–5523.
  • Amital H., Heilweil-Harel M., Ulmansky R., . Antibodies against the VRT101 laminin epitope correlate with human SLE disease activity and can be removed by extracorporeal immunoadsorption. Rheumatology (Oxford). 2007; 46 9: 1433–1437.
  • Li Q. Z., Xie C., Wu T., . Identification of autoantibody clusters that best predict lupus disease activity using glomerular proteome arrays. J. Clin. Invest.. 2005; 115 12: 3428–3439.
  • Fitzsimons M. M., Chen H., Foster M. H.. Diverse endogenous light chains contribute to basement membrane reactivity in nonautoimmune mice transgenic for an anti-laminin Ig heavy chain. Immunogenetics. 2000; 51:20–29.
  • Rudolph E. H., Congdon K. L., Sackey F. N., Fitzsimons M. M., Foster M. H.. Humoral autoimmunity to basement membrane antigens is regulated in C57BL/6 and MRL/MpJ mice transgenic for anti-laminin Ig receptors. J. Immunol.. 2002; 168:5943–5953.
  • Brady G. F., Congdon K. L., Clark A. G., . Kappa editing rescues autoreactive B cells destined for deletion in mice transgenic for a dual specific anti-laminin Ig. J. Immunol.. 2004; 172 9: 5313–5321.
  • Clark A. G., Mackin K. M., Foster M. H.. Tracking differential gene expression in MRL/MpJ versus C57BL/6 anergic B cells: Molecular markers of autiommunity. Biomarker Insights. 2008; 3:335–350.
  • Foster M. H., Fitzsimons M. M.. Lupus-like nephrotropic autoantibodies in nonautoimmune mice harboring an anti-basement membrane/anti-DNA Ig heavy chain transgene. Mol. Immunol.. 1998; 35:83–94.
  • Clark A. G., Mackin K. M., Foster M. H.. Genetic elimination of alpha3(IV) collagen fails to rescue anti-collagen B cells. Immunol. Lett.. 2011; 141 1: 134–139.
  • Oi V., Morrison S. L., Herzenberg L. A., Berg P.. Immunglobulin gene expression in transformed lymphoid cells. Proc. Natl. Acad. Sci. USA. 1983; 80:825–829.
  • Tybulewicz V. L. J., Crawford C. E., Jackson P. K., Bronson R. T., Mulligan R. C.. Neonatal lethality and lymphopenia in mice with a homozygous disruption of the c-abl proto-oncogene. Cell. 1991; 65:1153–1163.
  • Brochet X., Lefranc M.-P., Giudicelli V.. IMGT/V-Quest: the highly customized and integrated system for IG and TR standardized V-J and V-D-J sequence analysis. Nucl. Acids Res.. 2008; 36:W503–W508 doi: 10.1093.
  • Foster M. H., Cooperstone B. G., Chen H.. Anti-idiotypic monoclonal Ig specific for an anti-laminin Ig heavy chain transgene variable region. Hybridoma. 1998; 17 4: 323–329.
  • Amano H., Amano E., Moll T., . The Yaa mutation promoting murine lupus causes defective development of marginal zone B cells. J. Immunol.. 2003; 170 5: 2293–2301.
  • Moll T., Martinez-Soria E., Santiago-Raber M.-L., . Differential activation of anti-erythrocyte and anti-DNA autoreactive B lymphocytes by the Yaa mutation. J. Immunol.. 2005; 174:702–709.
  • Pisitkun P., Deane J. A., Difilippantonio M. J., . Difilippantonio et al. 2006. Autoreactive B cell responses to RNA-related antigens due to TLR7 gene duplication. Science. 2006; 312 5780: 1669–1672.
  • Subramanian S., Tus K., Li Q. Z., . A Tlr7 translocation accelerates systemic autoimmunity in murine lupus. Proc. Natl. Acad. Sci. USA. 2006; 103 26: 9970–9975.
  • Santiago-Raber M.-L., Kikuchi S., Borel P., . Evidence for genes in addition to Tlr7 in the Yaa translocation linked with acceleration of systemic lupus erythematosus. J. Immunol.. 2008; 181:1556–1562.
  • Meffre E.. The establishment of early B cell tolerance in humans: lessons from primary immunodeficiency diseases. Ann. NY Acad. Sci.. 2011; 1246 1: 1–10.
  • Isnardi I., Ng Y. S., Srdanovic I., . IRAK-4- and MyD88-dependent pathways are essential for the removal of developing autoreactive B cells in humans. Immunity. 2008; 29 5: 746–757.
  • Meyers G., Ng Y. S., Bannock J. M., . Activation-induced cytidine deaminase (AID) is required for B-cell tolerance in humans. Proc. Natl. Acad. Sci. USA. 2011; 108 28: 11554–11559.
  • Kuraoka M., Holl T. M., Liao D., . Activation-induced cytidine deaminase mediates central tolerance in B cells. Proceedings of the Natl. Acad. USA. 2011; 108 28: 11560–11565.
  • Menard L., Saadoun D., Isnardi I., . The PTPN22 allele encoding an R620W variant interferes with the removal of developing autoreactive B cells in humans. J. Clin. Invest.. 2011; 121 9: 3635–3644.
  • Murakami M., Tsubata T., Okamoto M., . Antigen-induced apoptotic death of Ly-1 B cells responsible for autoimmune disease in transgenic mice. Nature. 1992; 357:77–80.
  • Nisitani S., Sakiyama T., Honjo T.. Involvement of IL-10 in induction of autoimmune hemolytic anemia in anti-erythrocyte Ig transgenic mice. Int. Immunol.. 1998; 10 8: 1039–1047.
  • Goodnow C. C., Crosbie J., Adelstein S., . Altered immunoglobulin expression and functional silencing of self-reactive B lymphocytes in transgenic mice. Nature. 1988; 334:676–682.
  • Chang N.-H., Cheung Y.-H., Loh C., . B Cell activating factor (BAFF) and T cells cooperate to breach B cell tolerance in lupus-prone New Zealand Black (NZB) mice. PLoS One. 2010; 5 7: e11691.
  • Santiago-Raber M. L., Amano H., Amano E., . Evidence that Yaa-induced loss of marginal zone B cells is a result of dendritic cell-mediated enhanced activation. J. Autoimmun.. 2010; 34 4: 349–355.
  • Bendelac A., Bonneville M., Kearney J. F.. Autoreactivity by design: innate B and T lymphocytes. Nat. Rev. Immunol.. 2001; 1 3: 177–186.
  • Meyer-Bahlburg A., Rawlings D. J.. Differential impact of Toll-like receptor signaling on distinct B cell subpopulations. Front. Biosci.. 2012; 17:1499–1516.
  • Grimaldi C. M., Michael D. J., Diamond B.. Cutting edge: expansion and activation of a population of autoreactive marginal zone B cells in a model of estrogen-induced lupus. J. Immunol.. 2001; 167 4: 1886–1890.
  • Mackay F., Woodcock S. A., Lawton P., . Mice transgenic for BAFF develop lymphocytic disorders along with autoimmune manifestations. J. Exp. Med.. 1999; 190 11: 1697–1710.
  • Liu Y., Li L., Kumar K. R., . Lupus susceptibility genes may breach tolerance to DNA by impairing receptor editing of nuclear antigen-reactive B cells. J. Immunol.. 2007; 179 2: 1340–1352.
  • Duan B., Croker B. P., Morel L.. Lupus resistance is associated with marginal zone abnormalities in an NZM murine model. Lab. Invest. J. Tech. Meth. Pathol.. 2007; 87 1: 14–28.
  • Duan B., Niu H., Xu Z., . Intrafollicular location of marginal zone/CD1d(hi) B cells is associated with autoimmune pathology in a mouse model of lupus. Lab. Invest.. 2008; 88 9: 1008–1020.
  • Shao W. H., Kuan A. P., Wang C., . Disrupted Mer receptor tyrosine kinase expression leads to enhanced MZ B-cell responses. J. Autoimmun.. 2010; 35 4: 368–374.
  • Zhou Z., Niu H., Zheng Y. Y., Morel L.. Autoreactive marginal zone B cells enter the follicles and interact with CD4+T cells in lupus-prone mice. BMC Immunol.. 2011; 12:7.
  • Wither J. E., Loh C., Lajoie G., . Colocalization of expansion of the splenic marginal zone population with abnormal B cell activation and autoantibody production in B6 mice with an introgressed New Zealand Black chromosome 13 interval. J. Immunol.. 2005; 175 7: 4309–4319.
  • Foster M. H., Zhang Y., Clark A. G.. Deconstructing B cell tolerance to basement membranes. Arch. Immunol. Ther. Exp.. 2006; 54:227–237.
  • Al-Qahtani A., Xu Z., Zan H., Walsh C. M., Casali P.. A role for DRAK2 in the germinal center reaction and the antibody response. Autoimmunity. 2008; 41 5: 341–352.
  • Wellmann U., Letz M., Schneider A., Amann K., Winkler T. H.. An Ig mu-heavy chain transgene inhibits systemic lupus erythematosus immunopathology in autoimmune (NZB × NZW)F1 mice. Int. Immunol.. 2001; 13 12: 1461–1469.
  • Jacob N., Stohl W.. Autoantibody-dependent and autoantibody-independent roles for B cells in systemic lupus erythematosus: past, present, and future. Autoimmunity. 2010; 43 1: 84–97.
  • Roark J. H., Kuntz C. L., Nguyen K., Caton A. J., Erikson J.. Breakdown of B cell tolerance in a mouse model of systemic lupus erythematosus. J. Exp. Med.. 1995; 181:1157–1167.
  • Rubio C. F., Kench J., Russell D. M., Yawger R., Nemazee D.. Analysis of central B cell tolerance in autoimmune-prone MRL/lpr mice bearing autoantibody transgenes. J. Immunol.. 1996; 157:65–71.
  • Santulli-Marotto S., Qian Y., Ferguson S., Clarke S. H.. Anti-Sm B cell differentiation in Ig transgenic MRL/Mp-lpr/lpr mice: Altered differentiation and an accelerated response. J. Immunol.. 2001; 166 8: 5292–5299.
  • Chen C., Li H., Tian Q., . Selection of anti-double-stranded DNA B cells in autoimmune MRL-lpr/lpr mice. J. Immunol.. 2006; 176 9: 5183–5190 PubMed PMID: 16621982.
  • Friedmann D., Yachimovich N., Mostoslavsky G., . Production of high affinity autoantibodies in autoimmune New Zealand Black/New Zealand white F1 mice targeted with an anti-DNA heavy chain. J. Immunol.. 1999; 162:4406–4416.
  • Wellmann U., Werner A., Winkler T. H.. Altered selection processes of B lymphocytes in autoimmune NZB/W mice, despite intact central tolerance against DNA. Eur. J. Immunol.. 2001; 31:2800–2810.
  • Spatz L., Saenko V., Iliev A., . Light chain usage in anti-double-stranded DNA B cell subsets: Role in cell fate determination. J. Exp. Med.. 1997; 185:1317–1326.
  • Steeves M. A., Marion T. N.. Tolerance to DNA in (NZB x NZW)F1 mice that inherit an anti-DNA V(H) as a conventional micro H chain transgene but not as a V(H) knock-in transgene. J. Immunol.. 2004; 172 11: 6568–6577.
  • Duong B. H., Ota T., Ait-Azzouzene D., . Peripheral B cell tolerance and function in transgenic mice expressing an IgD superantigen. J. Immunol.. 2010; 184 8: 4143–4158.
  • Roes J., Rajewsky K.. Immunoglobulin D (IgD)-deficient mice reveal an auxiliary receptor function for IgD in antigen-mediated recruitment of B cells. J. Exper. Med.. 1993; 177 1: 45–55.
  • Nitschke L., Kosco M. H., Kohler G., Lamers M. C.. Immunoglobulin D-deficient mice can mount normal immune responses to thymus-independent and -dependent antigens. Proc. Natl. Acad. Sci. USA. 1993; 90 5: 1887–1891.
  • Woodward E. J., Thomas J. W.. Multiple germline kappa light chains generate anti-insulin B cells in nonobese diabetic mice. J. Immunol.. 2005; 175 2: 1073–1079.
  • Henry R. A., Kendall P. L., Woodward E. J., Hulbert C., Thomas J. W.. Vkappa polymorphisms in NOD mice are spread throughout the entire immunoglobulin kappa locus and are shared by other autoimmune strains. Immunogenetics. 2010; 62 8: 507–520.
  • Trepicchio W.Jr., Barrett K. J.. The Igh-V locus of MRL mice: Restriction fragment length polymorphism in eleven strains of mice as determined with VH and D gene probes. J. Immunol.. 1985; 134:2734–2739.
  • Kompfner E., Oliveira P., Montalbano A., Feeney A. J.. Unusual germline DSP2 gene accounts for all apparent V-D-D-J rearrangements in newborn, but not adult, MRL mice. J. Immunol.. 2001; 167 12: 6933–6938.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.