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Rosa, Domenico; Giulietta Saletti; De Gregorio, Ennio; Francesca Zorat; Consuelo Comar; D'Oro, Ugo; Nuti, Sandra; Houghton, Michael; Vincenzo Barnaba; Gabriele Pozzato; Abrignani, Sergio; Rappuoli, Rino
Proceedings of the National Academy of Sciences - PNAS, 12/2005, Letnik: 102, Številka: 51Journal Article
Infection with hepatitis C virus (HCV), a leading cause of chronic liver diseases, can associate with B lymphocyte proliferative disorders, such as mixed cryoglobulinemia and non-Hodgkin lymphoma. The major envelope protein of HCV (HCV-E2) binds, with high affinity CD81, a tetraspanin expressed on several cell types. Here, we show that engagement of CD81 on human B cells by a combination of HCV-E2 and an anti-CD81 mAb triggers the JNK pathway and leads to the preferential proliferation of the $na\ddot{i}ve$ (CD27-) B cell subset. In parallel, we have found that B lymphocytes from the great majority of chronic hepatitis C patients are activated and that $na\ddot{i}ve$ cells display a higher level of activation markers than memory (CD27+) B lymphocytes. Moreover, eradication of HCV infection by IFN therapy is associated with normalization of the activation-markers expression. We propose that CD81-mediated activation of B cells in vitro recapitulates the effects of HCV binding to B cell CD81 in vivo and that polyclonal proliferation of $na\ddot{i}ve$ B lymphocytes is a key initiating factor for the development of the HCV-associated B lymphocyte disorders.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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in: SICRIS
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