Peripheral Blood Lymphocyte Phenotype Differentiates Secondary Antibody Deficiency in Rheumatic Disease from Primary Antibody Deficiency

Journal of Clinical Medicine

卷:9

Faranaz Atschekzei¹  Georgios Sogkas¹  Haress Etemadi¹  Ignatius Ryan Adriawan²  Torsten Witte²  Roland Jacobs²  Sabine Buyny²  Diana Ernst²  Reinhold Ernst Schmidt² 

[1] ;

[2] Department of Rheumatology and Immunology, Hannover Medical School, 30625 Hannover, Germany;

关键词: hypogammaglobulinemia;    secondary hypogammaglobulinemia;    primary immunodeficiency;    common variable immunodeficiency;    methotrexate;    DMARD;   

DOI  :  10.3390/jcm9041049

来源: DOAJ

【 摘 要 】

The phenotype of primary immunodeficiency disorders (PID), and especially common variable immunodeficiency (CVID), may be dominated by symptoms of autoimmune disorders. Furthermore, autoimmunity may be the first manifestation of PID, frequently preceding infections and the diagnosis of hypogammaglobulinemia, which occurs later on. In this case, distinguishing PID from hypogammaglobulinemia secondary to anti-inflammatory treatment of autoimmunity may become challenging. The aim of this study was to evaluate the diagnostic accuracy of peripheral blood lymphocyte phenotyping in resolving the diagnostic dilemma between primary and secondary hypogammaglobulinemia. Comparison of B and T cell subsets from patients with PID and patients with rheumatic disease, who developed hypogammaglobulinemia as a consequence of anti-inflammatory regimes, revealed significant differences in proportion of naïve B cells, class-switched memory B cells and CD21^low B cells among B cells as well as in CD4⁺ memory T cells and CD4⁺ T follicular cells among CD4⁺ T cells. Identified differences in B cell and T cell subsets, and especially in the proportion of class-switched memory B cells and CD4⁺ T follicular cells, display a considerable diagnostic efficacy in distinguishing PID from secondary hypogammaglobulinemia due to anti-inflammatory regimens for rheumatic disease.

【 授权许可】

Unknown