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Genetic and Immunological Pathogenesis of Atopic Dermatitis
被引:8
|作者:
Schuler, Charles F.
[1
,2
]
Tsoi, Lam C.
[2
,3
]
Billi, Allison C.
[3
]
Harms, Paul W.
[3
,4
]
Weidinger, Stephan
[5
]
Gudjonsson, Johann E.
[2
,3
]
机构:
[1] Univ Michigan, Michigan Med, Dept Internal Med, Div Allergy & Clin Immunol, Ann Arbor, MI USA
[2] Univ Michigan, Michigan Med, Mary H Weiser Food Allergy Ctr, Ann Arbor, MI USA
[3] Univ Michigan, Michigan Med, Dept Dermatol, 6427C Med Sci Bldg I,1301 E Catherine St, Ann Arbor, MI 48109 USA
[4] Univ Michigan, Michigan Med, Dept Pathol, Ann Arbor, MI USA
[5] Univ Hosp Schleswig Holstein, Dept Dermatol Venereol & Allergol, Kiel, Germany
基金:
美国国家卫生研究院;
关键词:
Atopic dermatitis;
Epidermal barrier;
Epithelial barrier;
Genetics;
GWAS;
GENOME-WIDE ASSOCIATION;
OF-FUNCTION VARIANTS;
COPY-NUMBER VARIATION;
SUSCEPTIBILITY LOCI;
FILAGGRIN GENE;
DENDRITIC CELLS;
DOUBLE-BLIND;
RISK-FACTOR;
T-CELLS;
MODERATE;
D O I:
10.1016/j.jid.2023.10.019
中图分类号:
R75 [皮肤病学与性病学];
学科分类号:
100206 ;
摘要:
Type 2 immune-mediated diseases give a clear answer to the issue of nature (genetics) versus nurture (environment). Both genetics and environment play vital complementary roles in the development of atopic dermatitis (AD). As a key component of the atopic march, AD demonstrates the interactive nature of genetic and environmental contributions to atopy. From sequence variants in the epithelial barrier gene encoding FLG to the hygiene hypothesis, AD combines a broad array of contributions into a single syndrome. This review will focus on the genetic contribution to AD and where genetics facilitates the elicitation or enhancement of AD pathogenesis.
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页码:954 / 968
页数:15
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