The Immune Modulatory Effect of Allergen Specific Immunotherapy in Treated Asthmatics | ||||
Bulletin of Egyptian Society for Physiological Sciences | ||||
Article 4, Volume 28, Issue 1, June 2008, Page 33-46 PDF (250.86 K) | ||||
Document Type: Original Article | ||||
DOI: 10.21608/besps.2008.36814 | ||||
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Authors | ||||
E Fouda* 1; S Abd El Fatah2; M Barakat2; Lubna Anees3 | ||||
1Department of Internal Medicine, Al-Azhar University | ||||
2Department of Biochemistry Faculty of Pharmacy - Cairo University | ||||
3The National Center for Radiation Research and Technology | ||||
Abstract | ||||
Apoptosis is programmed cell death without induction of an inflammatory response. It is mediated by Fas–a cell surface protein which is expressed on activated lymphocytes. Interaction with its counterpart- the FasL induces the apoptosis of Fas bearing cells. The mechanismunderlying successful immunotherapy has not been identified. The aim of the present work was to investigate whether immunotherapy affect Fas expression on T lymphocytes in asthmatic patients and to investigate its potential ability to shift the Th1/Th2 balance ofimmune response to allergic reaction in asthmatic airway. The study was conducted on 30 asthmatic subjects and 10 healthy control subjects. The asthmatic patients were treated with immunotherapy for more than one year. Blood samples were collected at basal time (before treatment) and one year after therapy (the end of the building up phase). The percentage of positive T cells expressing Fas on its surface was determined using flow cytometryic analysis technique. The expression of Fas on asthmatic patients was significantly higher than in control subjects which decreases after immunotherapy but showing no evidence of apoptosis, levels of IgE, IL-4 were decreased significantly after treatment, also, level of IFN-γwas increased significantly.Conclusion:although high percentage of the Fas expressed in studied asthmatic group but with no clear evidence of apoptosis, may be a non concomitant increase in FasL which interfere with the apoptotic process in such asthmatics and might be a contributing factor in asthma pathogenesis. Thus, the lack of parallel increase of FasL to the increased Fas could explain the impaired apoptosis of the T- lymphocytes. It could be concluded that immunotherapy have a role in skewing the cytokine profile in asthma and maintain the balance between Th1/Th2. | ||||
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