| First Author | Yen MH | Year | 2002 |
| Journal | J Immunol | Volume | 169 |
| Issue | 2 | Pages | 722-31 |
| PubMed ID | 12097374 | Mgi Jnum | J:77746 |
| Mgi Id | MGI:2182511 | Doi | 10.4049/jimmunol.169.2.722 |
| Citation | Yen MH, et al. (2002) Induction of CD4 T cell changes in murine AIDS is dependent on costimulation and involves a dysregulation of homeostasis. J Immunol 169(2):722-31 |
| abstractText | Strong CD4 T cell activation and proliferation are seen in susceptible mice infected with the murine retroviral inoculum, LP-BM5, which produces an immunodeficiency syndrome called murine AIDS (MAIDS). We developed a short term adoptive transfer model of MAIDS to examine the requirements for the CD4 T cell response. Naive CD4 T cells from uninfected donors responded quickly after adoptive transfer into MAIDS-infected hosts, becoming activated and proliferating within several days. Using blocking mAbs to costimulatory ligands and CD4 T cells deficient in expression of their receptors, we found that the CD4 T cell response requires CD28:B7.1/B7.2 interactions, but not CTLA4 or CD40-CD40 ligand interactions. Naive CD4 T cells did not respond in H-2M-deficient mice with MAIDS, suggesting that disease requires recognition of self peptide-MHC complexes. The self MHC-dependent division and accumulation of large numbers of CD4 T cells suggest that MAIDS involves a disruption of the balance of homeostatic signals. Supporting this hypothesis, CD4 T cells from mice with MAIDS failed to regulate the homeostatic division of naive CD4 T cells in a cotransfer model. Thus, a combination of up-regulation of costimulatory ligands and disruption of homeostatic control may be responsible for CD4 lymphoproliferation in MAIDS. |
