| First Author | Moro M | Year | 2002 |
| Journal | Eur J Immunol | Volume | 32 |
| Issue | 12 | Pages | 3566-75 |
| PubMed ID | 12516542 | Mgi Jnum | J:292872 |
| Mgi Id | MGI:6435893 | Doi | 10.1002/1521-4141(200212)32:12<3566::AID-IMMU3566>3.0.CO;2-O |
| Citation | Moro M, et al. (2002) Blockade of CD86 in BALB/c mice infected with Leishmania major does not prevent the expansion of low avidity T cells. Eur J Immunol 32(12):3566-75 |
| abstractText | The interactions between CD28 and its ligand CD86 are critical for the regulation of T cell responses. However, it is not clear whether CD4+ T cells expressing low and high avidity TCR are equally dependent on CD28 costimulation for their activation and expansion. To address this issue, we have used multimers of I-Ad molecules linked to a peptide derived from the Leishmania major homolog for the receptor of activated C kinase (LACK) antigen to compare the fate of LACK-specific CD4+ T cells in Leishmania-infected BALB/c mice which have been treated or not with anti-CD86 mAb. Although the administration of anti-CD86 mAb did not completely prevent the expansion of LACK-specific T cells, their frequency and number were markedly reduced. In mice treated with anti-CD86 mAb as well as in control animals, L. major induced the clonal expansion of LACK-specific T cells which expressed a canonical low avidity Valpha8/Vbeta4 TCR. Taken together, our results suggest that the molecular interactions between CD28 on T cells and CD86 on APC serve to amplify and modulate T cell responses without promoting breadth in the TCR repertoire. |
