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Dermatology researchers have uncovered differences in the genetic architecture of psoriatic arthritis (PsA) and cutaneous psoriasis (PsC).
Dr. Philip E. Stuart of the University of Michigan, Ann Arbor, and his colleagues from 32 institutions in the United States, Europe, and Canada, carried out a genome-wide association study (GWAS) of 1,430 patients with psoriatic arthritis and 1,417 healthy controls. They then combined results of their GWAS with five published studies of psoriasis associations (three GWASs and two targeted studies), comprising 3,061 psoriatic arthritis patients, 3,110 cutaneous-only psoriasis patients, and 9,273 psoriasis vulgaris patients, and 13,670 healthy controls of European descent.
The work, published in the American Journal of Human Genetics, identified five regions of significance in the PsA GWAS. These were all in known risk regions for PsA, with the strongest signals near HLA-B, IL12B, TRAF3IP2, TNIP1, and TYK2.
Looking across all studies, researchers detected 10 regions associated with PsA and 11 with PsC at genome-wide significance. Several of these association signals (IFNLR1, IFIH1, NFKBIA for PsA, and TJFRSF9, LCE3C/B, TRAF3IP2, IL23A, and NFKBIA for PsC) had not previously achieved such significance. Researchers also identified a genetic variant associated with psoriasis vulgaris (PsV) near CDKAL1, and other variants that were more strongly associated with either PsA or PsC.
“These results provide insights into the pathogenic similarities and differences between PsC and PsA,” the authors wrote. Identifying the causative variants driving the observed associations “will aid prediction and therapy of psoriasis and its cutaneous and joint manifestations.”
Read the article in the American Journal of Human Genetics (2015 Dec 3;97:816-36).
Dermatology researchers have uncovered differences in the genetic architecture of psoriatic arthritis (PsA) and cutaneous psoriasis (PsC).
Dr. Philip E. Stuart of the University of Michigan, Ann Arbor, and his colleagues from 32 institutions in the United States, Europe, and Canada, carried out a genome-wide association study (GWAS) of 1,430 patients with psoriatic arthritis and 1,417 healthy controls. They then combined results of their GWAS with five published studies of psoriasis associations (three GWASs and two targeted studies), comprising 3,061 psoriatic arthritis patients, 3,110 cutaneous-only psoriasis patients, and 9,273 psoriasis vulgaris patients, and 13,670 healthy controls of European descent.
The work, published in the American Journal of Human Genetics, identified five regions of significance in the PsA GWAS. These were all in known risk regions for PsA, with the strongest signals near HLA-B, IL12B, TRAF3IP2, TNIP1, and TYK2.
Looking across all studies, researchers detected 10 regions associated with PsA and 11 with PsC at genome-wide significance. Several of these association signals (IFNLR1, IFIH1, NFKBIA for PsA, and TJFRSF9, LCE3C/B, TRAF3IP2, IL23A, and NFKBIA for PsC) had not previously achieved such significance. Researchers also identified a genetic variant associated with psoriasis vulgaris (PsV) near CDKAL1, and other variants that were more strongly associated with either PsA or PsC.
“These results provide insights into the pathogenic similarities and differences between PsC and PsA,” the authors wrote. Identifying the causative variants driving the observed associations “will aid prediction and therapy of psoriasis and its cutaneous and joint manifestations.”
Read the article in the American Journal of Human Genetics (2015 Dec 3;97:816-36).
Dermatology researchers have uncovered differences in the genetic architecture of psoriatic arthritis (PsA) and cutaneous psoriasis (PsC).
Dr. Philip E. Stuart of the University of Michigan, Ann Arbor, and his colleagues from 32 institutions in the United States, Europe, and Canada, carried out a genome-wide association study (GWAS) of 1,430 patients with psoriatic arthritis and 1,417 healthy controls. They then combined results of their GWAS with five published studies of psoriasis associations (three GWASs and two targeted studies), comprising 3,061 psoriatic arthritis patients, 3,110 cutaneous-only psoriasis patients, and 9,273 psoriasis vulgaris patients, and 13,670 healthy controls of European descent.
The work, published in the American Journal of Human Genetics, identified five regions of significance in the PsA GWAS. These were all in known risk regions for PsA, with the strongest signals near HLA-B, IL12B, TRAF3IP2, TNIP1, and TYK2.
Looking across all studies, researchers detected 10 regions associated with PsA and 11 with PsC at genome-wide significance. Several of these association signals (IFNLR1, IFIH1, NFKBIA for PsA, and TJFRSF9, LCE3C/B, TRAF3IP2, IL23A, and NFKBIA for PsC) had not previously achieved such significance. Researchers also identified a genetic variant associated with psoriasis vulgaris (PsV) near CDKAL1, and other variants that were more strongly associated with either PsA or PsC.
“These results provide insights into the pathogenic similarities and differences between PsC and PsA,” the authors wrote. Identifying the causative variants driving the observed associations “will aid prediction and therapy of psoriasis and its cutaneous and joint manifestations.”
Read the article in the American Journal of Human Genetics (2015 Dec 3;97:816-36).
FROM AMERICAN JOURNAL OF HUMAN GENETICS
