Gennady V Poryadin, Natalia E Zhuravleva, Jean M Salmasi, Alexander N Kazimirsky, Ludmila Yu Semenova, Sergei A Polner, Tatyana A Chervinskaya
{"title":"Immunological mechanisms of recovery from an acute stage in patients with atopic bronchial asthma.","authors":"Gennady V Poryadin, Natalia E Zhuravleva, Jean M Salmasi, Alexander N Kazimirsky, Ludmila Yu Semenova, Sergei A Polner, Tatyana A Chervinskaya","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>We have conducted a comparative study of the lymphocyte surface antigens in patients with atopic bronchial asthma (ABA) in an acute stage and during clinical remission of the disease using a wide variety of monoclonal antibodies. In patients with ABA, independently of the stage of the disease, we have observed a decline in the total number of T lymphocytes due to cell reduction in both sub-populations--T helpers and cytotoxic T cells. During the acute phase of the disease a significant increase in the number of B lymphocytes at all stages of differentiation was observed. This suggests a general activation of the B cell network of the immune system. In patients at all the phases of the disease we observed a statistically significant elevation in the number of activated B cells (CD23+) and of early activation markers CD25 and CD71, as well as of the lymphocytes that express the adhesion receptor CD54 (ICAM-1). On the contrary, a two-fold increase in the number of blood HLA DR lymphocytes was typical only for the patients in an acute phase of the disease. A significant increase in the activation parameters representing the CD25/CD95 and HLA DR/CD95 ratio was found during the ABA aggravation. Based on the obtained results we conclude that the development of the remission in ABA is associated with the restoration of the activation induced apoptosis of the lymphocytes, which in turn leads to a reduction in the intensity of the reagin response.</p>","PeriodicalId":21507,"journal":{"name":"Russian journal of immunology : RJI : official journal of Russian Society of Immunology","volume":"7 3","pages":"259-64"},"PeriodicalIF":0.0000,"publicationDate":"2002-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Russian journal of immunology : RJI : official journal of Russian Society of Immunology","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
We have conducted a comparative study of the lymphocyte surface antigens in patients with atopic bronchial asthma (ABA) in an acute stage and during clinical remission of the disease using a wide variety of monoclonal antibodies. In patients with ABA, independently of the stage of the disease, we have observed a decline in the total number of T lymphocytes due to cell reduction in both sub-populations--T helpers and cytotoxic T cells. During the acute phase of the disease a significant increase in the number of B lymphocytes at all stages of differentiation was observed. This suggests a general activation of the B cell network of the immune system. In patients at all the phases of the disease we observed a statistically significant elevation in the number of activated B cells (CD23+) and of early activation markers CD25 and CD71, as well as of the lymphocytes that express the adhesion receptor CD54 (ICAM-1). On the contrary, a two-fold increase in the number of blood HLA DR lymphocytes was typical only for the patients in an acute phase of the disease. A significant increase in the activation parameters representing the CD25/CD95 and HLA DR/CD95 ratio was found during the ABA aggravation. Based on the obtained results we conclude that the development of the remission in ABA is associated with the restoration of the activation induced apoptosis of the lymphocytes, which in turn leads to a reduction in the intensity of the reagin response.