Author/Authors :
Tang، نويسنده , , Yao and Kim، نويسنده , , Wan Kee and Holmes، نويسنده , , Kevin L. and Hügin، نويسنده , , Ambros W. and Kenny، نويسنده , , James J. and Chattopadhyay، نويسنده , , Sisir K. and Hartley، نويسنده , , Janet W. and Morse III، نويسنده , , Herbert C.، نويسنده ,
Abstract :
C57BL/6 (B6) mice develop a syndrome of progressive lymphoproliferation and immunodeficiency, murine AIDS (MAIDS), when infected with an etiologic replication-defective virus termed BM5def. Induction of MAIDS requires the presence of CD4+ T cells and B cells. B6 mice with altered conventional B cell function and a deficit in CD5+ B cells due to the xid mutation develop disease with a greatly prolonged latency. The association of this mutation with resistance to MAIDS was confirmed in studies of Pxid mice. To test the hypothesis that conventional B cells are required for rapid induction of disease, B6xid mice were injected with spleen cells from nude mice or were given hone marrow from aged donors. Both sets of recipients developed advanced disease by 10 weeks post infection, suggesting that resistance to MAIDS in xid mutants may be due to effects of B cells other than the CD5+ subset.
