Genomic alterations driving psoriasis pathogenesis

被引：53
|
作者：
Singh, S. [1 ]
Pradhan, D. [1 ,2 ]
Puri, P. [3 ]
Ramesh, V. [3 ]
Aggarwal, S. [1 ,4 ]
Nayek, A. [1 ]
Jain, A. K. [1 ]
机构：
[1] Natl Inst Pathol ICMR, Biomed Informat Ctr, New Delhi 110029, India
[2] Indian Council Med Res, ICMR AIIMS Computat Genom Ctr, New Delhi 110029, India
[3] Safdarjang Hosp, Dermatol Dept, New Delhi 110029, India
[4] AIIMS, Dept Biochem, Raipur, Chhattisgarh, India
来源：
GENE | 2019年 / 683卷
关键词：
Genetic triggers; Keratinocytes; Autoimmunity; IL23/Type 17 T cell axis; PSORS; PLACEBO-CONTROLLED TRIAL; JANUS KINASE INHIBITOR; PLAQUE-TYPE PSORIASIS; QUALITY-OF-LIFE; INTERLEUKIN-12/23; MONOCLONAL-ANTIBODY; COPY NUMBER VARIATIONS; HLA-C; DOUBLE-BLIND; IN-VITRO; MODERATE;
D O I：
10.1016/j.gene.2018.09.042
中图分类号：
Q3 [遗传学];
学科分类号：
071007 ; 090102 ;
摘要：
Psoriasis is an immune mediated inflammatory skin disease with complex etiology involving interplay between environmental and genetic risk factors as disease initiating event. Enhanced understanding on genetic risk factors, differentially expressed genes, deregulated proteins and pathway-targeted therapeutics have established multiple axis of psoriasis pathogenesis. So far, loci in 424 genes are reported to be associated with psoriasis alongside copy number variations and epigenetic alterations. From clinical perspective, presence of specific genetic trigger(s) in individual psoriasis patient could aid in devising a personalized therapeutic strategy. Therefore, the review presents an updates on reported genomic alterations and their subsequent course of cutaneous inflammations that potentially drive to psoriasis.
引用
收藏
页码：61 / 71
页数：11
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