A regulatory polymorphism in PDCD1 is associated with susceptibility to systemic lupus erythematosus in humans
(2002) In Nature Genetics 32(4). p.666-669- Abstract
- Systemic lupus erythematosus (SLE, OMIM 152700) is a complex autoimmune disease that affects 0.05% of the Western population, predominantly women(1-4). A number of susceptibility loci for SLE have been suggested in different populations, but the nature of the susceptibility genes and mutations is yet to be identified(5-9). We previously reported a susceptibility locus (SLEB2) for Nordic multi-case families(9,10). Within this locus, the programmed cell death 1 gene (PDCD1, also called PD-1) was considered the strongest candidate for association with the disease(11-14). Here, we analyzed 2,510 individuals, including members of five independent sets of families as well as unrelated individuals affected with SLE, for single-nucleotide... (More)
- Systemic lupus erythematosus (SLE, OMIM 152700) is a complex autoimmune disease that affects 0.05% of the Western population, predominantly women(1-4). A number of susceptibility loci for SLE have been suggested in different populations, but the nature of the susceptibility genes and mutations is yet to be identified(5-9). We previously reported a susceptibility locus (SLEB2) for Nordic multi-case families(9,10). Within this locus, the programmed cell death 1 gene (PDCD1, also called PD-1) was considered the strongest candidate for association with the disease(11-14). Here, we analyzed 2,510 individuals, including members of five independent sets of families as well as unrelated individuals affected with SLE, for single-nucleotide polymorphisms (SNPs) that we identified in PDCD1. We show that one intronic SNP in PDCD1 is associated with development of SLE in Europeans (found in 12% of affected individuals versus 5% of controls; P=0.00001, r.r. (relative risk)=2.6) and Mexicans (found in 7% of affected individuals versus 2% of controls; P=0.0009, r.r.=3.5). The associated allele of this SNP alters a binding site for the runt-related transcription factor 1 (RUNX1, also called AML1) located in an intronic enhancer, suggesting a mechanism through which it can contribute to the development of SLE in humans. (Less)
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https://lup.lub.lu.se/record/322191
- author
- organization
- publishing date
- 2002
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Nature Genetics
- volume
- 32
- issue
- 4
- pages
- 666 - 669
- publisher
- Nature Publishing Group
- external identifiers
-
- pmid:12402038
- wos:000179593000022
- scopus:13244277850
- ISSN
- 1546-1718
- DOI
- 10.1038/ng1020
- language
- English
- LU publication?
- yes
- id
- ada7db0a-aab0-4645-990e-1c470f2248d5 (old id 322191)
- date added to LUP
- 2016-04-01 16:52:33
- date last changed
- 2022-04-23 00:55:04
@article{ada7db0a-aab0-4645-990e-1c470f2248d5, abstract = {{Systemic lupus erythematosus (SLE, OMIM 152700) is a complex autoimmune disease that affects 0.05% of the Western population, predominantly women(1-4). A number of susceptibility loci for SLE have been suggested in different populations, but the nature of the susceptibility genes and mutations is yet to be identified(5-9). We previously reported a susceptibility locus (SLEB2) for Nordic multi-case families(9,10). Within this locus, the programmed cell death 1 gene (PDCD1, also called PD-1) was considered the strongest candidate for association with the disease(11-14). Here, we analyzed 2,510 individuals, including members of five independent sets of families as well as unrelated individuals affected with SLE, for single-nucleotide polymorphisms (SNPs) that we identified in PDCD1. We show that one intronic SNP in PDCD1 is associated with development of SLE in Europeans (found in 12% of affected individuals versus 5% of controls; P=0.00001, r.r. (relative risk)=2.6) and Mexicans (found in 7% of affected individuals versus 2% of controls; P=0.0009, r.r.=3.5). The associated allele of this SNP alters a binding site for the runt-related transcription factor 1 (RUNX1, also called AML1) located in an intronic enhancer, suggesting a mechanism through which it can contribute to the development of SLE in humans.}}, author = {{Prokunina, L and Castillejo-Lopez, C and Oberg, F and Gunnarsson, I and Berg, L and Magnusson, V and Brookes, AJ and Tentler, D and Kristjansdottir, H and Grondal, G and Bolstad, AI and Svenungsson, E and Lundberg, I and Sturfelt, Gunnar and Jonssen, A and Truedsson, Lennart and Lima, G and Alcocer-Varela, J and Jonsson, R and Gyllensten, UB and Harley, JB and Alarcon-Segovia, D and Steinsson, K and Alarcon-Riquelme, ME}}, issn = {{1546-1718}}, language = {{eng}}, number = {{4}}, pages = {{666--669}}, publisher = {{Nature Publishing Group}}, series = {{Nature Genetics}}, title = {{A regulatory polymorphism in PDCD1 is associated with susceptibility to systemic lupus erythematosus in humans}}, url = {{http://dx.doi.org/10.1038/ng1020}}, doi = {{10.1038/ng1020}}, volume = {{32}}, year = {{2002}}, }