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2015 ; 64
(ä): 125-36
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Immunogenetics of systemic lupus erythematosus: A comprehensive review
#MMPMID26324017
Ghodke-Puranik Y
; Niewold TB
J Autoimmun
2015[Nov]; 64
(ä): 125-36
PMID26324017
show ga
Our understanding of the genetic basis of systemic lupus erythematosus has
progressed rapidly in recent years. While many genetic polymorphisms have been
associated with disease susceptibility, the next major step involves integrating
these genetic polymorphisms into the molecular mechanisms and cellular immunology
of the human disease. In this review, we summarize some recent work in this area,
including the genetics of the type I IFN response in SLE, including polygenic and
monogenic factors, as well as epigenetic influences. Contributions of both HLA
and non-HLA polymorphisms to the complex genetics of SLE are reviewed. We also
review recent reports of specific gene deficits leading to monogenic SLE-like
syndromes. The molecular functions of common SLE-risk variants are reviewed in
depth, including regulatory variations in promoter and enhancer elements and
coding-change polymorphisms, and studies which are beginning to define the
molecular and cellular functions of these polymorphisms in the immune system. We
discuss epigenetic influences on lupus, with an emphasis on micro-RNA expression
and binding, as well as epigenetic modifications that regulate the expression
levels of various genes involved in SLE pathogenesis and the ways epigenetic
marks modify SLE susceptibility genes. The work summarized in this review
provides a fascinating window into the biology and molecular mechanisms of human
SLE. Understanding the functional mechanisms of causal genetic variants
underlying the human disease greatly facilitates our ability to translate genetic
associations toward personalized care, and may identify new therapeutic targets
relevant to human SLE disease mechanisms.
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