Mohammadi Nejad Mozafar, Salehi Eisa, Mesdaghi Mehrnaz, Atarod Lida, Movahedi Masoud, Gheflati Zahra, Aboufazeli Tahereh, Vodjgani Mohammad
Department of Immunology, Mofid Children Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Iran J Allergy Asthma Immunol. 2013 Mar;12(1):68-74.
Allergic rhinitis (AR) is an inflammatory disorder of the nasal mucosa with high morbidity and prevalence. Natural killer (NK) cells might have a role in AR. We aimed to evaluate the changes of the markers and receptors on NK cells in AR patients compared to the non-atopic controls.Flow cytometric analysis was used with double staining of the Peripheral Blood Mononuclear Cells (PBMCs) to examine the expression of CD25 and CD69 markers, and NKG2D and NKG2A receptors on NK cells of 20 patients with AR and 20 non-atopic controls. The serum total IgE level was measured by Enzyme-linked Immunosorbent Assay.The expression of CD69 antigen on NK cells in AR patients was significantly higher than that of healthy group (p=0.03). No significant changes were observed between CD25, NKG2D and NKG2A expression on the surface of NK cells from healthy and AR subjects. Our study also showed that there was no significant correlation between the expression of CD69, CD25, NKG2D and NKG2A and level of serum total IgE in AR patients and normal subjects.These results indicated that the expression of CD69 antigen on NK cells of AR patients was increased. The high expression of CD69 on NK cells in AR patients suggested that these cells were activated, probably due to the cytokines secreted from allergen-stimulated T cells and activated monocytes.
变应性鼻炎(AR)是一种鼻黏膜炎症性疾病,发病率和患病率都很高。自然杀伤(NK)细胞可能在AR中发挥作用。我们旨在评估AR患者与非特应性对照相比NK细胞上标志物和受体的变化。采用流式细胞术对外周血单个核细胞(PBMCs)进行双重染色,以检测20例AR患者和20例非特应性对照的NK细胞上CD25和CD69标志物以及NKG2D和NKG2A受体的表达。采用酶联免疫吸附测定法测定血清总IgE水平。AR患者NK细胞上CD69抗原的表达显著高于健康组(p = 0.03)。健康人和AR患者NK细胞表面的CD25、NKG2D和NKG2A表达之间未观察到显著变化。我们的研究还表明,AR患者和正常受试者中CD69、CD25、NKG2D和NKG2A的表达与血清总IgE水平之间无显著相关性。这些结果表明,AR患者NK细胞上CD69抗原的表达增加。AR患者NK细胞上CD69的高表达表明这些细胞被激活,可能是由于变应原刺激的T细胞和活化的单核细胞分泌的细胞因子所致。