| Literature DB >> 20832369 |
A Rensing-Ehl1, K Warnatz, S Fuchs, M Schlesier, U Salzer, R Draeger, I Bondzio, Y Joos, A Janda, M Gomes, M Abinun, S Hambleton, A Cant, F Shackley, T Flood, C Waruiru, K Beutel, K Siepermann, G Dueckers, T Niehues, T Wiesel, V Schuster, M G Seidel, M Minkov, K Sirkiä, M V Kopp, M Korhonen, K Schwarz, S Ehl, C Speckmann.
Abstract
Autoimmune lymphoproliferative syndrome (ALPS) is mainly caused by defects in the CD95 pathway. Raised CD3+TCRαβ+CD4-CD8- double negative T cells and impaired T cell apoptosis are hallmarks of the disease. In contrast, the B cell compartment has been less well studied. We found an altered distribution of B cell subsets with raised transitional B cells and reduced marginal zone B cells, switched memory B cells and plasma blasts in most of 22 analyzed ALPS patients. Moreover, 5 out of 66 ALPS patients presented with low IgG and susceptibility to infection revealing a significant overlap between ALPS and common variable immunodeficiency (CVID). In patients presenting with lymphoproliferation, cytopenia, hypogammaglobulinemia and impaired B cell differentiation, serum biomarkers were helpful in addition to apoptosis tests for the identification of ALPS patients. Our observations may indicate a role for apoptosis defects in some diseases currently classified as CVID.Entities:
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Year: 2010 PMID: 20832369 DOI: 10.1016/j.clim.2010.08.008
Source DB: PubMed Journal: Clin Immunol ISSN: 1521-6616 Impact factor: 3.969