| First Author | Bugeon L | Year | 2001 |
| Journal | Eur J Immunol | Volume | 31 |
| Issue | 1 | Pages | 118-27 |
| PubMed ID | 11169445 | Mgi Jnum | J:110947 |
| Mgi Id | MGI:3652440 | Doi | 10.1002/1521-4141(200101)31:1<118::aid-immu118>3.0.co;2-x |
| Citation | Bugeon L, et al. (2001) Selective silencing of full-length CD80 but not IgV-CD80 leads to impaired clonal deletion of self-reactive T cells and altered regulation of immune responses. Eur J Immunol 31(1):118-27 |
| abstractText | Co-stimulation provided by the B7 family of proteins underpins the development of protective immunity. There are three identified members of this family: CD80, its splice variant IgV-CD80 and CD86. It has hitherto been difficult to analyze the expression and function of IgV-CD80 since there are no appropriate reagents capable of distinguishing it from CD80. We have generated mice, by gene targeting, the lack CD80 whilst maintaining expression of IgV-CD80. Mutant animals did not delete T cells bearing mammary tumor virus-reactive TCR as efficiently as wild-type animals. We also demonstrate the importance of IgV-CD80 in the responses of recently activated cells and reveal a role for CD80 in sustaining T cell responses. CD86, whilst critical to primary T cell activation, made only a minor contribution to re-activation of normal cells. |
