| First Author | Havenar-Daughton C | Year | 2006 |
| Journal | J Immunol | Volume | 176 |
| Issue | 6 | Pages | 3315-9 |
| PubMed ID | 16517698 | Mgi Jnum | J:129538 |
| Mgi Id | MGI:3769629 | Doi | 10.4049/jimmunol.176.6.3315 |
| Citation | Havenar-Daughton C, et al. (2006) Cutting Edge: The direct action of type I IFN on CD4 T cells is critical for sustaining clonal expansion in response to a viral but not a bacterial infection. J Immunol 176(6):3315-9 |
| abstractText | The action of type I IFN (IFN-I) on APCs is well studied, but their direct effect on CD4 T cells is unclear. To address this, we transferred IFN-I receptor-deficient (IFN-IR(0)) and -sufficient (wild-type, WT) TCR-transgenic CD4 T cells into WT mice and analyzed their response to immunization. In response to lymphocytic choriomeningitis virus immunization, WT CD4 T cells expanded approximately 100-fold, whereas IFN-IR(0) CD4 T cells expanded <10-fold. However, both WT and IFN-IR(0) CD4 T cells expanded approximately 10-fold after Listeria monocytogenes immunization. Poor expansion of IFN-IR(0) CD4 T cells after lymphocytic choriomeningitis virus immunization was not due to a defect in proliferation or initial activation but to poor survival of the daughter cells. Thus, direct IFN-I signals can play either a critical or minimal role in CD4 T cell clonal expansion depending on the specific pathogen. |
