| First Author | Numata F | Year | 1997 |
| Journal | Int Immunol | Volume | 9 |
| Issue | 1 | Pages | 139-46 |
| PubMed ID | 9043955 | Mgi Jnum | J:38501 |
| Mgi Id | MGI:85884 | Doi | 10.1093/intimm/9.1.139 |
| Citation | Numata F, et al. (1997) The xid mutation plays an important role in delayed development of murine acquired immunodeficiency syndrome. Int Immunol 9(1):139-46 |
| abstractText | Infection of C57BL/6 mice with LP-BM5 murine leukemia virus (MuLV) leads to the development of murine acquired immunodeficiency syndrome (MAIDS) characterized by abnormal lymphoproliferation, hypergammaglobulinemia and severe immunodeficiency, Progression of MAIDS is delayed in X chromosome-linked immunodeficient (XID) mice, which have an abnormality of Bruton's tyrosine kinase (Btk) and lack functionally mature B cells including CD5(+) B cells. In this study, we report the following four major findings, (i) Susceptibility to disease induction is not reconstituted by transfer of CD5(+) B cells to XID mice. (ii) Spleen cells from asymptomatic XID mice are able to transmit MAIDS to wild-type mice. (iii) MAIDS can be transmitted to XID mice with the transfer of B cells, but not T cells, from C57BL/6 mice with MAIDS. (iv) Cells which undergo massive lymphoproliferation in XID mice with MAIDS by cell transfer are of host origin, but are not from the donor. We suggest from these results that a B cell subpopulation that is impaired in XID mice plays an important role in the initiation of MAIDS. |
