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The genetics of Takayasu arteritis
#MMPMID28756073
Renauer P
; Sawalha AH
Presse Med
2017[Jul]; 46
(7-8 Pt 2
): e179-e187
PMID28756073
show ga
Takayasu arteritis (TAK) is a rare systemic vasculitis that is characterized by
granulomatous inflammation of the aorta and its major branches. The cellular and
biochemical processes involved in the pathogenesis of TAK are beginning to be
elucidated, and implicate both cell and antibody-mediated autoimmune mechanisms.
In addition, the underlying etiology to TAK may be explained, at least in part,
by a complex genetic contribution. The most well-recognized genetic
susceptibility locus for the disease is the classical HLA allele, HLA-B*52, which
has been confirmed in several ethnicities. The genetic susceptibility with
HLA-B*52, as well as additional classical alleles and loci, implicate both HLA
class I and class II involvement in TAK. Furthermore, genetic associations with
genes encoding immune response regulators, pro-inflammatory cytokines and
mediators of humoral immunity may directly relate to disease mechanisms. Non-HLA
susceptibility loci that have been recently established for TAK with a
genome-wide level of significance include FCGR2A/FCGR3A, IL12B, IL6, RPS9/LILRB3,
and a locus on chromosome 21 near PSMG1. In this review, we present the complex
genetic predisposition to TAK and discuss how recent findings identified
potential targets in the pathogenesis and treatment of the disease.
|Alleles
[MESH]
|Antigens, CD/genetics
[MESH]
|Genetic Predisposition to Disease
[MESH]
|Histocompatibility Antigens Class I/genetics
[MESH]
|Histocompatibility Antigens Class II/genetics
[MESH]
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