Progress towards understanding the genetic pathogenesis of systemic lupus erythematosus

Timothy W. Behrens; Robert R. Graham; Chieko Kyogoku; Emily C. Baechler; Paula S. Ramos; Clarence Gillett; Jason Bauer; Ward A. Ortmann; Keli L Hippen; Erik J Peterson; Carl D. Langefeld; Kathy L. Moser; Patrick M. Gaffney; Peter K. Gregersen

Progress towards understanding the genetic pathogenesis of systemic lupus erythematosus

Timothy W. Behrens, Robert R. Graham, Chieko Kyogoku, Emily C. Baechler, Paula S. Ramos, Clarence Gillett, Jason Bauer, Ward A. Ortmann, Keli L Hippen, Erik J Peterson, Carl D. Langefeld, Kathy L. Moser, Patrick M. Gaffney, Peter K. Gregersen

Research output: Chapter in Book/Report/Conference proceeding › Conference contribution

13 Scopus citations

Abstract

In order to better understand the genetic factors that initiate systemic lupus erythematosus (SLE), we are using both linkage and association approaches to identify susceptibility genes for the disease. Association studies have recently identified three HLA Class II haplotypes as well as a functional missense polymorphism in protein tyrosine phosphatase (PTP) PTPN22 as important risk alleles for SLE. Here, we will review these data, and explain how these findings contribute to an understanding of the genetic architecture of human SLE.

Original language	English (US)
Title of host publication	Genetics of Autoimmunity
Pages	145-160
Number of pages	16
State	Published - 2005

Publication series

Name	Novartis Foundation Symposium
Volume	267
ISSN (Print)	1528-2511

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Behrens, T. W., Graham, R. R., Kyogoku, C., Baechler, E. C., Ramos, P. S., Gillett, C., Bauer, J., Ortmann, W. A., Hippen, K. L., Peterson, E. J., Langefeld, C. D., Moser, K. L., Gaffney, P. M., & Gregersen, P. K. (2005). Progress towards understanding the genetic pathogenesis of systemic lupus erythematosus. In Genetics of Autoimmunity (pp. 145-160). (Novartis Foundation Symposium; Vol. 267).

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abstract = "In order to better understand the genetic factors that initiate systemic lupus erythematosus (SLE), we are using both linkage and association approaches to identify susceptibility genes for the disease. Association studies have recently identified three HLA Class II haplotypes as well as a functional missense polymorphism in protein tyrosine phosphatase (PTP) PTPN22 as important risk alleles for SLE. Here, we will review these data, and explain how these findings contribute to an understanding of the genetic architecture of human SLE.",

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AU - Graham, Robert R.

AU - Kyogoku, Chieko

AU - Baechler, Emily C.

AU - Ramos, Paula S.

AU - Gillett, Clarence

AU - Bauer, Jason

AU - Ortmann, Ward A.

AU - Hippen, Keli L

AU - Peterson, Erik J

AU - Langefeld, Carl D.

AU - Moser, Kathy L.

AU - Gaffney, Patrick M.

AU - Gregersen, Peter K.

PY - 2005

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N2 - In order to better understand the genetic factors that initiate systemic lupus erythematosus (SLE), we are using both linkage and association approaches to identify susceptibility genes for the disease. Association studies have recently identified three HLA Class II haplotypes as well as a functional missense polymorphism in protein tyrosine phosphatase (PTP) PTPN22 as important risk alleles for SLE. Here, we will review these data, and explain how these findings contribute to an understanding of the genetic architecture of human SLE.

AB - In order to better understand the genetic factors that initiate systemic lupus erythematosus (SLE), we are using both linkage and association approaches to identify susceptibility genes for the disease. Association studies have recently identified three HLA Class II haplotypes as well as a functional missense polymorphism in protein tyrosine phosphatase (PTP) PTPN22 as important risk alleles for SLE. Here, we will review these data, and explain how these findings contribute to an understanding of the genetic architecture of human SLE.

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M3 - Conference contribution

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AN - SCOPUS:27244455477

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BT - Genetics of Autoimmunity

ER -

Progress towards understanding the genetic pathogenesis of systemic lupus erythematosus

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