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   Phenotypic Study of Natural Killer Cell Subsets in Ankylosing Spondylitis Patients  
   
نویسنده Mousavi Tahereh ,Poormoghim Hadi ,Moradi Maziar ,Tajik Nader ,Shahsavar Farhad ,Soofi Mahboobeh
منبع iranian journal of allergy, asthma and immunology - 2009 - دوره : 8 - شماره : 4 - صفحه:193 -198
چکیده    It has been demonstrated that natural killer (nk) cells play a role in regulation ofautoimmunity. they play a protective role in several rodent disease models. in this study weaimed to compare the immunophenotypic features of nk cells in ankylosing spondylitis(as) with normal subjects with regard to cd56 and cd16 molecules.this study was carried out on 30 as patients and 33 normal volunteer donors. peripheralblood mononuclear cells (pbmc) were tested by flow cytometry detecting the intensity ofcd56 and cd16 surface molecules. the percentage of positive cells and their subsets werethen calculated and statistically analyzed using spss software. a significant increase wasfound in cd56+ cd16+ (p≤ 0.009), and also in the subset of cd56 dim cd16+ (p≤ 0.02), butnot in cd56 bright cd16+ (p=0.3) nk cells in as patients compared to controls. weconclude that these results may indicate that nk and their subset ratios play a role in aspathogenesis. moreover, determination of nk subsets in combination with clinical featuresmay be useful for as diagnosis. however, further studies using large samples together withdetermination of relevant cytokines are recommended to verify the exact role of nk in asdisease.
کلیدواژه Ankylosing Spondylitis; CD56; CD16; Natural Killer cell
آدرس iran university of medical sciences, Department of Immunology, ایران, iran university of medical sciences, Firooz-Gar Hospital, Rheumatology Department, ایران, iran university of medical sciences, Department of Social Medicine, ایران, iran university of medical sciences, Department of Immunology, ایران, Khorram- Abad University, Department of Immunology, ایران, iran university of medical sciences, Department of Immunology, ایران
پست الکترونیکی yasaha@iums.ac.ir
 
     
   
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