| First Author | Harris DP | Year | 2001 |
| Journal | J Immunol | Volume | 166 |
| Issue | 10 | Pages | 6041-9 |
| PubMed ID | 11342621 | Mgi Jnum | J:69348 |
| Mgi Id | MGI:1934479 | Doi | 10.4049/jimmunol.166.10.6041 |
| Citation | Harris DP, et al. (2001) B cell immunodeficiency fails to develop in cd4-deficient mice infected with bm5: murine aids as a multistep disease. J Immunol 166(10):6041-9 |
| abstractText | The immunodeficiency syndrome murine AIDS (MAIDS), caused by the BM5 retrovirus preparation, involves the activation, division, and subsequent anergy of the entire CD4(+) T cell population as well as extensive B cell hyperproliferation and hypergammaglobulinemia, resulting in splenomegaly and lymphadenopathy, followed many weeks later by death. The development of MAIDS requires CD4(+) T cells and MHC class II expression by the infected host, supporting a role for T-B interaction in disease development or progression. To explore this possibility, we examined development of MAIDS in mice deficient in CD4 (CD4 knockout), in which T-B interactions are compromised. We find that in CD4 knockout hosts, BM5 causes T cell immunodeficiency in the remaining T cells but has only a limited ability to induce B cell phenotypic changes, hyperproliferation, hypergammaglobulinemia, or splenomegaly. There is also delayed death of infected mice. This implies that CD4 dependent T-B interaction is needed to induce the B cell aspects of disease and supports a multistep mechanism of disease in which B cell changes follow and are caused by CD4(+) T cell effects. |
