KIR Allelic Variation and the Remission of Atopic Dermatitis Over Time.
KIR Allelic Variation and the Remission of Atopic Dermatitis Over Time.
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DOI：
10.4049/immunohorizons.2200095
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发表时间：
2023-01-01
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影响因子：
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通讯作者：
Phillips EJ
中科院分区：
文献类型：
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作者：
Margolis DJ;Mitra N;Hoffstad OJ;Chopra A;Phillips EJ
特应性皮炎是一种常见的慢性皮肤病。虽然通常被认为是一种T细胞调节失调的疾病，但最近的研究表明，NK细胞的免疫调节失调也很重要。杀伤细胞免疫球蛋白样受体(KIRS)参与NK细胞的调节。儿科湿疹选择性登记是一个美国全国性的纵向队列，对655名儿童进行了长达10年的随访，其中有DNA可用于全等位基因KIR测序。每隔6个月，由儿童湿疹选择性登记处报告AD活动。使用广义估计方程，我们评估了KIR等位基因变异与已知的人类白细胞抗原结合配体的相关性，以及儿童是否报告AD处于“缓解”状态(没有皮肤损害，也没有使用AD药物)。在C*04：01存在的情况下，KIR2DL4*001：01(优势比0.53，95%CI[0.32，0.88])和KIR2DL4*001：02(0.54，[0.33，0.89])对AD缓解的影响最大。单倍型KIR2DL4*001：02∼2DL4*001：01∼3DL2*002：01(0.77，[0.60，0.99])也与AD缓解的可能性降低相关。我们的发现增加了越来越多的文献关于NK细胞在AD的免疫发病机制和自然病程方面的重要性的证据。
Atopic dermatitis (AD) is a common chronic skin disease. Although generally thought to be a disease of T-cell dysregulation, recent studies have suggested that immune dysregulation of NK cells is also important. Killer cell Ig-like receptors (KIRs) are involved with NK cell regulation. The Pediatric Eczema Elective Registry is a U.S. nationwide longitudinal cohort with up to 10 y of follow-up in which 655 children had DNA available for full allelic KIR sequencing. Every 6 mo, AD activity was reported by Pediatric Eczema Elective Registry children. Using generalized estimating equations, we evaluated the association of KIR allelic variation in concert with known HLA binding ligands and whether the child reported AD in “remission” (no skin lesions and not using AD medication). KIR2DS4*001:01 (odds ratio 0.53, 95% CI [0.32, 0.88]) and KIR2DL4*001:02 (0.54, [0.33, 0.89]) in the presence of C*04:01 had the largest effect on decreasing the likelihood of AD remission. The haplotype KIR 2DL4*001:02 ∼ 2DS4*001:01 ∼ 3DL2*002:01 (0.77, [0.60, 0.99]) was also associated with a decreased likelihood of AD remission. Our findings add to the general body of evidence of a growing literature on the importance of NK cells with respect to the immunopathogenesis and natural history of AD.