PMID- 19758198
OWN - NLM
STAT- MEDLINE
DCOM- 20091029
LR  - 20221207
IS  - 1749-6632 (Electronic)
IS  - 0077-8923 (Linking)
VI  - 1173
DP  - 2009 Sep
TI  - Race differences in immunogenetic features and photosensitivity of cutaneous 
      lupus erythematosus from the aspect of Japanese studies.
PG  - 552-6
LID - 10.1111/j.1749-6632.2009.04676.x [doi]
AB  - Skin lesions of collagen diseases are influenced by environmental triggers, such 
      as UV light, and are variable in cutaneous lupus erythematosus (LE), such as 
      systemic LE (SLE), chronic discoid LE (CDLE), subacute cutaneous LE (SCLE), and 
      LE tumidus (LET). Although there are a few conflicting reports on 
      photosensitivity in collagen diseases, many Japanese dermatologists feel there 
      are photosensitivity differences in LE between Asians and Caucasians with SCLE 
      and LET. To address this issue, we have carried out genetic studies of Japanese 
      SLE and CDLE patients and reviewed the race differences in photosensitivity of 
      cutaneous LE from Japanese studies. Human leukocyte antigen (HLA) studies in 
      Japanese patients revealed that HLA-DRB1*1501 association was with CDLE and SLE. 
      The association between HLA-Cw6 and CDLE was first reported in a Japanese 
      population, and a HLA-A33-B44-DRB1*1302 haplotype showed a positive association 
      in CDLE. However, these results are not compatible with those from Caucasian 
      subjects. There are no significant associations among HLA studies, 
      photosensitivity, and anti-Ro/SS-A antibodies in Japanese CLE patients. 
      Photosensitivity will be a key factor to dissolve multifactorial complexes of LE 
      etiopathogenesis. An axis of photosensitivity, anti-Ro/SS-A antibodies, and 
      apoptosis via tumor necrosis factor-alpha is the best marker to verify the 
      contribution of genetics in CLE patients. The incidence and degree of 
      photosensitivity of SCLE and LET are much lower in Japanese than in Caucasians. 
      This discrepancy may lead to investigations of CLE pathogenesis through global 
      collaborations.
FAU - Furukawa, Fukumi
AU  - Furukawa F
AD  - Department of Dermatology, Wakayama Medical University, Wakayama, Japan. 
      dajs@wakayama-med.ac.jp
FAU - Yamamoto, Yuki
AU  - Yamamoto Y
FAU - Kanazawa, Nobuo
AU  - Kanazawa N
FAU - Muto, Masahiko
AU  - Muto M
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Ann N Y Acad Sci
JT  - Annals of the New York Academy of Sciences
JID - 7506858
RN  - 0 (HLA-A Antigens)
RN  - 0 (HLA-C Antigens)
RN  - 0 (HLA-C*06 antigen)
RN  - 0 (HLA-DR Antigens)
RN  - 0 (HLA-DRB1 Chains)
RN  - 0 (HLA-DRB1*15:01 antigen)
SB  - IM
MH  - Asian People/genetics
MH  - Chronic Disease
MH  - Gene Frequency
MH  - HLA-A Antigens/genetics
MH  - HLA-C Antigens/*genetics
MH  - HLA-DR Antigens/*genetics
MH  - HLA-DRB1 Chains
MH  - Haplotypes
MH  - Humans
MH  - Incidence
MH  - Japan/epidemiology
MH  - Lupus Erythematosus, Cutaneous/complications/ethnology/*genetics
MH  - Lupus Erythematosus, Discoid/complications/ethnology/*genetics
MH  - Photosensitivity Disorders/epidemiology/etiology/*pathology
MH  - White People/genetics
EDAT- 2009/09/18 06:00
MHDA- 2009/10/30 06:00
CRDT- 2009/09/18 06:00
PHST- 2009/09/18 06:00 [entrez]
PHST- 2009/09/18 06:00 [pubmed]
PHST- 2009/10/30 06:00 [medline]
AID - NYAS4676 [pii]
AID - 10.1111/j.1749-6632.2009.04676.x [doi]
PST - ppublish
SO  - Ann N Y Acad Sci. 2009 Sep;1173:552-6. doi: 10.1111/j.1749-6632.2009.04676.x.