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本文引用的文献

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Skewed distribution of natural killer cells in psoriasis skin lesions.银屑病皮损中自然杀伤细胞的分布偏倚。
Exp Dermatol. 2013 Jan;22(1):64-6. doi: 10.1111/exd.12060.
2
Autoimmune disease induction in a healthy human organ: a humanized mouse model of alopecia areata.在健康人体器官中诱导自身免疫性疾病:斑秃的人源化小鼠模型
J Invest Dermatol. 2013 Mar;133(3):844-847. doi: 10.1038/jid.2012.365. Epub 2012 Oct 25.
3
Psoriasis patients are enriched for genetic variants that protect against HIV-1 disease.银屑病患者中富含能预防 HIV-1 疾病的遗传变异。
PLoS Genet. 2012 Feb;8(2):e1002514. doi: 10.1371/journal.pgen.1002514. Epub 2012 Feb 16.
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The development of colitogenic CD4(+) T cells is regulated by IL-7 in collaboration with NK cell function in a murine model of colitis.在结肠炎的小鼠模型中,IL-7 与 NK 细胞功能协同调节致结肠炎 CD4(+)T 细胞的发育。
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Natural killer cell activation enhances immune pathology and promotes chronic infection by limiting CD8+ T-cell immunity.自然杀伤细胞的激活通过限制 CD8+T 细胞免疫来增强免疫病理并促进慢性感染。
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Natural killer cells act as rheostats modulating antiviral T cells.自然杀伤细胞充当调节抗病毒 T 细胞的变阻器。
Nature. 2011 Nov 20;481(7381):394-8. doi: 10.1038/nature10624.
7
Interleukin (IL)-17 versus IL-27: opposite effects on tumor necrosis factor-α-mediated chemokine production in human keratinocytes.白细胞介素 (IL)-17 与 IL-27:对人角质形成细胞中肿瘤坏死因子-α介导的趋化因子产生的相反作用。
Exp Dermatol. 2012 Jan;21(1):70-2. doi: 10.1111/j.1600-0625.2011.01384.x. Epub 2011 Nov 14.
8
NKG2C deletion is a risk factor of HIV infection.自然杀伤细胞2C(NKG2C)缺失是HIV感染的一个危险因素。
AIDS Res Hum Retroviruses. 2012 Aug;28(8):844-51. doi: 10.1089/AID.2011.0253. Epub 2012 May 3.
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NK cells and psoriasis.自然杀伤细胞与银屑病。
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10
HLA-E expression by gynecological cancers restrains tumor-infiltrating CD8⁺ T lymphocytes.妇科肿瘤的 HLA-E 表达抑制肿瘤浸润的 CD8⁺ T 淋巴细胞。
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在银屑病易感性中,NKG2C 激活受体的缺失及其配体 HLA-E 的功能多态性。

Deletion of the activating NKG2C receptor and a functional polymorphism in its ligand HLA-E in psoriasis susceptibility.

机构信息

Department of Dermatology, University of California San Francisco, San Francisco, CA, USA; Department of Dermatology, Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China.

出版信息

Exp Dermatol. 2013 Oct;22(10):679-81. doi: 10.1111/exd.12233.

DOI:10.1111/exd.12233
PMID:24079744
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3813441/
Abstract

Psoriasis is an inflammatory, immune-mediated disease of the skin. Several studies have suggested that natural killer (NK) cells and their receptors may be important for its pathogenesis. Here, we examined whether deletion of the activating natural killer receptor gene NKG2C, which has a frequency of 20% in the European population, was associated with psoriasis susceptibility. The NKG2C deletion and a functional polymorphism in its ligand HLA-E were genotyped in a Caucasian cohort of 611 psoriasis cases and 493 controls. We found that the NKG2C deletion was significantly increased in cases compared with controls [0.258 vs 0.200, P = 0.0012, OR = 1.43 (1.15-1.79)]. The low-expressing HLA-E*01:01 allele was associated with psoriasis (P = 0.0018), although this association was dependent on HLA-C. Our findings support a potential immunoregulatory role for NK cells in psoriasis and suggest the importance of future studies to investigate the contribution of NK cells and their regulatory receptors to the pathogenesis of psoriasis.

摘要

银屑病是一种皮肤炎症性、免疫介导的疾病。多项研究表明,自然杀伤(NK)细胞及其受体可能对其发病机制具有重要作用。在这里,我们研究了在欧洲人群中频率为 20%的激活型自然杀伤细胞受体基因 NKG2C 的缺失是否与银屑病易感性有关。我们在一个由 611 例银屑病病例和 493 例对照组成的白种人队列中对 NKG2C 缺失和其配体 HLA-E 的功能多态性进行了基因分型。我们发现,与对照组相比,病例组中 NKG2C 缺失明显增加[0.258 比 0.200,P = 0.0012,OR = 1.43(1.15-1.79)]。低表达的 HLA-E*01:01 等位基因与银屑病有关(P = 0.0018),尽管这种关联依赖于 HLA-C。我们的研究结果支持 NK 细胞在银屑病中的潜在免疫调节作用,并表明未来研究调查 NK 细胞及其调节受体对银屑病发病机制的贡献的重要性。