| First Author | Weintraub JP | Year | 1999 |
| Journal | Clin Immunol | Volume | 91 |
| Issue | 3 | Pages | 302-9 |
| PubMed ID | 10370375 | Mgi Jnum | J:55186 |
| Mgi Id | MGI:1337464 | Doi | 10.1006/clim.1999.4717 |
| Citation | Weintraub JP, et al. (1999) Ectopic expression of B7-1 (CD80) on T lymphocytes in autoimmune lpr and gld mice. Clin Immunol 91(3):302-9 |
| abstractText | Defective Fas-mediated apoptosis in mice, caused by the gld mutation in the fas ligand gene, results in the development of lupus-like autoantibodies and severe lymphoproliferation. We previously demonstrated ectopic expression of the costimulatory molecule B7-1 (CD80) on T lymphocytes in B6/gld mice. This report extends these observations by demonstrating similar results in B6/lpr mice, which possess a mutation in the gene encoding Fas, Additionally, we demonstrate that this phenomenon is age- dependent and occurs on multiple subsets of B6/gld T lymphocytes. B7-1 upregulation is observed on T cells from both conventionally housed and specific-pathogen-free B6/gld mice, suggesting that this is not a consequence of infection by pathogen. T cells from lpr and gld mice show increased binding of CTLA4-Ig fusion protein, suggesting that the upregulated B7-1 is functional. CD28, a receptor for B7-1 which activates T cells, is upregulated in B6/lpr and B6/gld mice, while CTLA4, a negative regulator of T cells which binds B7-1, is not. Our results suggest that ectopic expression of B7-1 on T cells of lpr and gld mice may be playing: a role in exacerbation of lymphoproliferation and/or autoimmunity. (C) 1999 Academic Press. |
