| First Author | Poudrier J | Year | 2001 |
| Journal | Immunity | Volume | 15 |
| Issue | 2 | Pages | 173-85 |
| PubMed ID | 11520454 | Mgi Jnum | J:131516 |
| Mgi Id | MGI:3773833 | Doi | 10.1016/s1074-7613(01)00177-7 |
| Citation | Poudrier J, et al. (2001) The AIDS disease of CD4C/HIV transgenic mice shows impaired germinal centers and autoantibodies and develops in the absence of IFN-gamma and IL-6. Immunity 15(2):173-85 |
| abstractText | The mechanisms responsible for degeneration of germinal centers (GC) and follicular dendritic cell (FDC) networks during progression to AIDS remain elusive. Here, we show that CD4(+) T cells from CD4C/HIV-1 Tg mice, which develop a severe AIDS-like disease, express low levels of CD40 ligand. Accordingly, GC formation, FDC networks, and immunoglobulin isotype switching are impaired in these animals. However, Tg B cells respond to in vitro CD40 stimulation. Total serum IgG levels are reduced in Tg mice, whereas total IgM levels are increased with a significant amount showing DNA specificity. IFN-gamma- and IL-6-deficient CD4C/HIV Tg mice also develop the AIDS-like disease and produce auto-Ab. Thus, CD4C/HIV Tg mice have immune dysfunction accompanied by autoimmune responses. |
