PMID- 23380467
OWN - NLM
STAT- MEDLINE
DCOM- 20131101
LR  - 20130409
IS  - 1095-9157 (Electronic)
IS  - 0896-8411 (Linking)
VI  - 41
DP  - 2013 Mar
TI  - Immunologic and genetic considerations of cutaneous lupus erythematosus: a 
      comprehensive review.
PG  - 34-45
LID - S0896-8411(13)00008-5 [pii]
LID - 10.1016/j.jaut.2013.01.007 [doi]
AB  - Cutaneous lupus erythematosus (CLE) refers to those subtypes of lupus 
      erythematosus (LE) that have predominantly skin manifestations. Discoid lupus 
      erythematosus (DLE), subacute cutaneous lupus erythematosus (SCLE), LE 
      panniculitis (LEP) and lupus erythematosus tumidus (LET) all fall into the 
      category of CLE. The pathogenesis of CLE is likely multifactorial. UV irradiation 
      has been shown to induce keratinocyte apoptosis. Impaired clearance of apoptotic 
      cells is a potential mechanism for the development of CLE. UV irradiation can 
      also induce externalization of autoantigens such as Ro/SSA, exposing them to 
      circulating autoantibodies. Some drugs have been associated with CLE. Possible 
      mechanisms include stimulation of an immune response through disruption of 
      central tolerance and altered T cell function. T17 cells may also play a role in 
      the pathogenesis of CLE as they have been detected in skin lesions of LE. Treg 
      cells have been found to be decreased in LE lesions, which may contribute to the 
      breakdown of self-tolerance. Epidermal Langerhans cells are reduced in CLE while 
      plasmacytoid DCs are increased in the lesions of CLE, suggesting that DCs may 
      also play an important role in the pathogenesis of CLE. Type I IFN- and TNF-alpha are 
      both upregulated in lesions of CLE. Other cytokines such as IL-6 and IL-17 are 
      also implicated in the pathogenesis of CLE. Cellular and cytokine networks can be 
      impacted by environmental factors and genetic variations and this can result in 
      an increased risk of developing autoimmune diseases such as CLE.
CI  - Copyright (c) 2013 Elsevier Ltd. All rights reserved.
FAU - Yu, Cong
AU  - Yu C
AD  - Department of Dermatology, Peking University People's Hospital, No. 11 Xizhimen 
      South Street, Beijing 100044, China.
FAU - Chang, Christopher
AU  - Chang C
FAU - Zhang, Jianzhong
AU  - Zhang J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20130201
PL  - England
TA  - J Autoimmun
JT  - Journal of autoimmunity
JID - 8812164
RN  - 0 (Cytokines)
SB  - IM
MH  - Cytokines/genetics/immunology/metabolism
MH  - Gene Expression/immunology
MH  - Humans
MH  - Lupus Erythematosus, Cutaneous/*genetics/*immunology
MH  - Models, Genetic
MH  - Models, Immunological
MH  - Skin/*immunology/*metabolism/pathology
MH  - T-Lymphocytes/immunology/metabolism
EDAT- 2013/02/06 06:00
MHDA- 2013/11/02 06:00
CRDT- 2013/02/06 06:00
PHST- 2013/01/04 00:00 [received]
PHST- 2013/01/04 00:00 [accepted]
PHST- 2013/02/06 06:00 [entrez]
PHST- 2013/02/06 06:00 [pubmed]
PHST- 2013/11/02 06:00 [medline]
AID - S0896-8411(13)00008-5 [pii]
AID - 10.1016/j.jaut.2013.01.007 [doi]
PST - ppublish
SO  - J Autoimmun. 2013 Mar;41:34-45. doi: 10.1016/j.jaut.2013.01.007. Epub 2013 Feb 1.