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2 results on '"Scherbarth, H.R."'

1. Chromosome 17p12-q11 harbors susceptibility loci for systemic lupus erythematosus

Author

Johansson, C.M. Zunec, R. Garía, M.A. Scherbarth, H.R. Tate, G.A. Paira, S. Navarro, S.M. Perandones, C.E. Gamron, S. Alvarellos, A. Graf, C.E. Manni, J. Berbotto, G.A. Palatnik, S.A. Catoggio, L.J. Battagliotti, C.G. Sebastiani, G.D. Migliaresi, S. Galeazzi, M. Pons-Estel, B.A. Alarcón-Riquelme, M.E. Gunnarsson, I. Svennungson, E. Gordon, C. Jonsson, R. Moutsopoulos, H. Doria, A. Marcos, J.C. Marcos, A.I. Marino, P.C. Motta, E.L. Allevi, A. Presas, J.L. Roverano, A. Louteiro, C. Ramos, F.A. Prigione, C.S. Eimon, A. Drenkard, C. Menso, E. Caeiro, F. Bertoli, A. Caprarulo, C. Buchanan, G. Bertero, E. Grimaudo, S. Guillersn, C. Jorfen, M. Romero, E.J. Abdala, M. Bearzotti, M. Soriano, E.R. Santos, C.D. Battagliotti, C.A.

Abstract

Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by the presence of autoantibodies against intracellular components, the formation of immune complexes, and inflammation in various organs, typically the skin and kidney glomeruli. The etiology of the disease is not well understood but is most likely the result of the interaction between genetic and environmental factors. In order to identify susceptibility loci for SLE, we have performed genome scans with microsatellite markers covering the whole genome in families from Argentina, Italy, and Europe. The results reveal a heterogeneous disease with different susceptibility loci in different family sets. We have found significant linkage to chromosome 17p12-q11 in the Argentine set of families. The maximum LOD score was given by marker D17S1294 in combination with D17S1293, when assuming a dominant inheritance model (Z=3.88). We also analyzed a repeat in the promoter region of the NOS2A gene, a strong candidate gene in the region, but no association was found. The-locus on chromosome 17 has © Springer-Verlag 2004.

Published
2004

2. Kallikrein genes are associated with lupus and glomerular basement membrane-specific antibody-induced nephritis in mice and humans

Author

Liu, Kui, Li, Quan-Zhen, Delgado-Vega, Angelica M., Abelson, Anna-Karin, Sánchez, Elena, Kelly, Jennifer A., Li, Li, Liu, Yang, Zhou, Jinchun, Yan, Mei, Ye, Qiu, Liu, Shenxi, Xie, Chun, Zhou, Xin J., Chung, Sharon A., Pons-Estel, Bernardo, Witte, Torsten, de Ramón, Enrique, Bae, Sang-Cheol, Barizzone, Nadia, Sebastiani, Gian Domenico, Merrill, Joan T., Gregersen, Peter K., Gilkeson, Gary G., Kimberly, Robert P., Vyse, Timothy J., Kim, Il, D'Alfonso, Sandra, Martin, Javier, Harley, John B., Criswell, Lindsey A., Wakeland, Edward K., Alarcón-Riquelme, Marta E., Mohan, Chandra, Danieli, M.G., Galeazzi, M., Querini, P.R., Migliaresi, S., Scherbarth, H.R., Lopez, J.A., Motta, E.L., Gamron, S., Drenkard, C., Menso, E., Allievi, A., Tate, G.A., Presas, J.L., Palatnik, S.A., Abdala, M., Bearzotti, M., Alvarellos, A., Caeiro, F., Bertoli, A., Paira, S., Roverano, S., Graf, C.E., Bertero, E., Caprarulo, C., Buchanan, G., Guillerón, C., Grimaudo, S., Manni, J., Catoggio, L.J., Soriano, E.R., Santos, C.D., Prigione, C., Ramos, F.A., Navarro, S.M., Berbotto, G.A., Jorfen, M., Romero, E.J., Garcia, M.A., Marcos, J.C., Marcos, A.I., Perandones, C.E., Eimon, A., Battagliotti, C.G., Armadi-Simab, K., Gross, W.L., Gromica-Ihle, E., Peter, H.H., Manger, K., Schnarr, S., Zeidler, H., Schmidt, R.E., Ortego, N., Callejas, J.L., Jiménez-Alonso, J., Sabio, M., Sánchez-Román, J., Garcia-Hernandez, F.J., Camps, M., López-Nevot, M.A., González-Escribano, M.F., Harley, J.H., Riquelme, M.A., Kimberly, R., Criswell, L., Langefeld, C., Tsao, B., Jacob, C., Liu, Kui, Li, Quan-Zhen, Delgado-Vega, Angelica M., Abelson, Anna-Karin, Sánchez, Elena, Kelly, Jennifer A., Li, Li, Liu, Yang, Zhou, Jinchun, Yan, Mei, Ye, Qiu, Liu, Shenxi, Xie, Chun, Zhou, Xin J., Chung, Sharon A., Pons-Estel, Bernardo, Witte, Torsten, de Ramón, Enrique, Bae, Sang-Cheol, Barizzone, Nadia, Sebastiani, Gian Domenico, Merrill, Joan T., Gregersen, Peter K., Gilkeson, Gary G., Kimberly, Robert P., Vyse, Timothy J., Kim, Il, D'Alfonso, Sandra, Martin, Javier, Harley, John B., Criswell, Lindsey A., Wakeland, Edward K., Alarcón-Riquelme, Marta E., Mohan, Chandra, Danieli, M.G., Galeazzi, M., Querini, P.R., Migliaresi, S., Scherbarth, H.R., Lopez, J.A., Motta, E.L., Gamron, S., Drenkard, C., Menso, E., Allievi, A., Tate, G.A., Presas, J.L., Palatnik, S.A., Abdala, M., Bearzotti, M., Alvarellos, A., Caeiro, F., Bertoli, A., Paira, S., Roverano, S., Graf, C.E., Bertero, E., Caprarulo, C., Buchanan, G., Guillerón, C., Grimaudo, S., Manni, J., Catoggio, L.J., Soriano, E.R., Santos, C.D., Prigione, C., Ramos, F.A., Navarro, S.M., Berbotto, G.A., Jorfen, M., Romero, E.J., Garcia, M.A., Marcos, J.C., Marcos, A.I., Perandones, C.E., Eimon, A., Battagliotti, C.G., Armadi-Simab, K., Gross, W.L., Gromica-Ihle, E., Peter, H.H., Manger, K., Schnarr, S., Zeidler, H., Schmidt, R.E., Ortego, N., Callejas, J.L., Jiménez-Alonso, J., Sabio, M., Sánchez-Román, J., Garcia-Hernandez, F.J., Camps, M., López-Nevot, M.A., González-Escribano, M.F., Harley, J.H., Riquelme, M.A., Kimberly, R., Criswell, L., Langefeld, C., Tsao, B., and Jacob, C.

Abstract

Immune-mediated nephritis contributes to disease in systemic lupus erythematosus, Goodpasture syndrome (caused by antibodies specific for glomerular basement membrane [anti-GBM antibodies]), and spontaneous lupus nephritis. Inbred mouse strains differ in susceptibility to anti-GBM antibody-induced and spontaneous lupus nephritis. This study sought to clarify the genetic and molecular factors that maybe responsible for enhanced immune-mediated renal disease in these models. When the kidneys of 3 mouse strains sensitive to anti-GBM antibody-induced nephritis were compared with those of 2 control strains using microarray analysis, one-fifth of the underexpressed genes belonged to the kallikrein gene family,which encodes serine esterases. Mouse strains that upregulated renal and urinary kallikreins exhibited less evidence of disease. Antagonizing the kallikrein pathway augmented disease, while agonists dampened the severity of anti-GBM antibody-induced nephritis. In addition, nephritis-sensitive mouse strains had kallikrein haplotypes that were distinct from those of control strains, including several regulatory polymorphisms,some of which were associated with functional consequences. Indeed, increased susceptibility to anti-GBM antibody-induced nephritis and spontaneous lupus nephritis was achieved by breeding mice with a genetic interval harboring the kallikrein genes onto a disease-resistant background. Finally, both human SLE and spontaneous lupus nephritis were found to be associated with kallikrein genes, particularly KLK1 and the KLK3 promoter, when DNA SNPs from independent cohorts of SLE patients and controls were compared. Collectively, these studies suggest that kallikreins are protective disease-associated genes in anti-GBM antibody-induced nephritis and lupus.

Published
2009
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