Autor: |
Koenen PG; Department of Immunology, University Medical Center, Lundlaan 6, 3584 EA Utrecht, The Netherlands., Hofhuis FM, Oosterwegel MA, Tesselaar K |
Jazyk: |
angličtina |
Zdroj: |
Journal of immunology (Baltimore, Md. : 1950) [J Immunol] 2007 May 01; Vol. 178 (9), pp. 5762-8. |
DOI: |
10.4049/jimmunol.178.9.5762 |
Abstrakt: |
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. |
Databáze: |
MEDLINE |
Externí odkaz: |
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