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GWAS Study

Whole-genome sequencing reveals rare and structural variants contributing to psoriasis and identifies CERCAM as a risk gene.

Sonehara K, Watanabe R, Matsumura Y et al.

40848718 PubMed ID
GWAS Study Type
5383 Participants
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Chapter I

Publication Details

Comprehensive information about this research publication

Authors

SK
Sonehara K
WR
Watanabe R
MY
Matsumura Y
MY
Mitsui Y
OY
Ogawa Y
OK
Odomari K
SS
Sakaue S
NS
Namba S
KM
Komuro M
EM
Edamoto M
WJ
Watanabe J
HT
Hirota T
AN
Arase N
NY
Nakamura Y
NK
Nakajima K
OT
Okamoto T
NR
Nishikawa R
YK
Yamamoto K
SK
Suzuki K
KT
Kishikawa T
ER
Edahiro R
SY
Shirai Y
NT
Naito T
SN
Sasa N
IY
Ishitsuka Y
FJ
Furuta J
KK
Kunimoto K
KI
Kajihara I
FS
Fukushima S
MH
Miyachi H
MH
Matsue H
KM
Kamata M
MM
Momose M
MI
Miyagawa I
TH
Tanaka H
UM
Ueno M
BT
Bito T
NH
Nagai H
IT
Ikeda T
HT
Horikawa T
AA
Adachi A
MT
Matsubara T
NE
Nishida E
MK
Matsuda K
SN
Shojima N
NI
Nakagawa I
AY
Asano Y
SS
Sato S
IS
Imafuku S
TY
Tada Y
NC
Nishigori C
JM
Jinnin M
IH
Ihn H
AA
Asahina A
SH
Saeki H
YT
Yamauchi T
KT
Kadowaki T
KT
Kawamura T
SS
Shimada S
KI
Katayama I
HK
Higasa K
NE
Noguchi E
SS
Sano S
TY
Tanaka Y
MF
Matsuda F
KA
Kumanogoh A
TM
Tamari M
ST
Satoh T
FM
Fujimoto M
MA
Morita A
OY
Okada Y
Chapter II

Abstract

Summary of the research findings

Psoriasis vulgaris (PsV) is an immune-mediated inflammatory skin disorder with complex genetic architecture. Most genome-wide association studies (GWASs) of PsV have been limited to analyzing common single-nucleotide variants in Europeans, lacking diversity in the variant spectrum and ancestral background. To investigate the contribution of rare variants (RVs) and structural variants (SVs), we perform a whole-genome sequencing study involving 1,415 PsV cases and 3,968 controls in Japanese. A GWAS signal at IFNLR1 is fine-mapped to a 3.3-kb deletion SV disrupting an epithelium-specific putative enhancer, which is validated by PacBio long-read sequencing. Gene-based RV analyses identify two susceptibility genes: IFIH1 (p = 9.8 × 10-6) and CERCAM (p = 4.1 × 10-7). Notably, IL36RN, a causative gene for generalized pustular psoriasis, a rare and lethal multi-systemic inflammatory disorder, is associated with common PsV (p = 1.2 × 10-4). Finally, Cercam knockout (Cercam-/-) in an imiquimod-induced psoriasis mouse model aggravates dermatitis with elevated T cell retention in the subepidermis. Our study elucidates the overlooked genetic basis of PsV.

1,415 Japanese ancestry cases, 3,968 Japanese ancestry controls

Chapter III

Study Statistics

Key metrics and study information

5383
Total Participants
GWAS
Study Type
No
Replicated
East Asian
Ancestry
Japan
Recruitment Country
Chapter IV

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