First Author | Koenen PG | Year | 2007 |
Journal | J Immunol | Volume | 178 |
Issue | 9 | Pages | 5762-8 |
PubMed ID | 17442960 | Mgi Jnum | J:145832 |
Mgi Id | MGI:3836127 | Doi | 10.4049/jimmunol.178.9.5762 |
Citation | Koenen PG, et al. (2007) T cell activation and proliferation characteristic for HIV-Nef transgenic mice is lymphopenia induced. J Immunol 178(9):5762-8 |
abstractText | The HIV-Nef protein has been implicated in generating high viral loads and T cell activation. Transgenic (tg) mice with constitutive T cell-specific Nef expression show a dramatic reduction in T cell number and highly increased T cell turnover. Previous studies in Nef tg mice attributed this T cell activation to a direct effect of Nef at the cellular level. Given the strongly reduced peripheral T cell numbers, we examined whether this enhanced T cell division might instead be lymphopenia induced. Adoptively transferred naive wild-type T cells into lymphopenic Nef tg mice showed high T cell turnover and obtained the same effector/memory phenotype as the autologous Nef tg T cells, supporting the idea that the microenvironment determines the phenotype of the T cells present. Moreover, in bone marrow chimeras from mixtures of wild-type and Nef tg bone marrow, with a full T cell compartment containing a small proportion of Nef tg T cells, Nef tg T cells kept a naive phenotype. These results demonstrate that T cell activation in the Nef tg mice is lymphopenia induced rather than due to a direct T cell-activating effect of Nef. |