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・ HLA-A80
・ HLA-A9
・ HLA-B
・ HLA-B associated transcript 3
・ HLA-B*82
・ HLA-B*83
・ HLA-B12
・ HLA-B13
・ HLA-B14
・ HLA-B15
・ HLA-B16
・ HLA-B17
・ HLA-B18
・ HLA-B21
・ HLA-B22
HLA-B27
・ HLA-B35
・ HLA-B37
・ HLA-B38
・ HLA-B39
・ HLA-B40
・ HLA-B41
・ HLA-B42
・ HLA-B44
・ HLA-B45
・ HLA-B46
・ HLA-B47
・ HLA-B48
・ HLA-B49
・ HLA-B5


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HLA-B27 : ウィキペディア英語版
HLA-B27

Human Leukocyte Antigen (HLA) B27 (subtypes B
*2701-2759) is a class I surface antigen encoded by the B locus in the major histocompatibility complex (MHC) on chromosome 6 and presents antigenic peptides (derived from self and non-self antigens) to T cells. HLA-B27 is strongly associated with ankylosing spondylitis (AS), and other associated inflammatory diseases referred to as "spondyloarthropathies".
The prevalence of HLA-B27 varies markedly in the general population. For example, about 8% of Caucasians, 4% of North Africans, 2-9% of Chinese, and 0.1-0.5% of persons of Japanese descent possess this gene.〔 In northern Scandinavia (Lapland), 24% of people are HLA-B27 positive, while 1.8% have associated ankylosing spondylitis.
A small group (<0.5%) of people infected with HIV are able to remain symptom-free for many years without medication. These "HIV controllers" appear to be slightly more common among people who are HLA-B27 positive.〔Deeks, S. G., Walker, B. D. Human Immunodeficiency Virus Controllers: Mechanisms of Durable Virus Control in the Absence of Antiretroviral Therapy. Immunity, 2007, 27: 406-416〕
==Disease associations==

The relationship between HLA-B27 and many diseases has not yet been fully elucidated. Though it is associated with a wide range of pathology, particularly seronegative spondyloarthropathy, it does not appear to be the sole mediator in development of disease. For example, while 90% of people with ankylosing spondylitis (AS) are HLA-B27 positive, only a fraction of people with HLA-B27 ever develop AS. Individuals who are HLA-B27 positive are more likely to experience early onset AS than HLA-B27 negative individuals. There are additional genes being discovered that also predispose to AS and associated diseases.〔Thomas GP, Brown MA. Genetics and Genomics of Ankylosing Spondylitis. Immunol Rev. 2010; 233:162-180.〕 Additionally there are potential environmental factors (triggers) that may also play a role in susceptible individuals.〔

抄文引用元・出典: フリー百科事典『 ウィキペディア(Wikipedia)
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