Autor: |
Goldrath AW; Department of Immunology and Howard Hughes Medical Institute, University of Washington, Seattle, Washington 98195, USA., Bogatzki LY, Bevan MJ |
Jazyk: |
angličtina |
Zdroj: |
The Journal of experimental medicine [J Exp Med] 2000 Aug 21; Vol. 192 (4), pp. 557-64. |
DOI: |
10.1084/jem.192.4.557 |
Abstrakt: |
In a depleted lymphoid compartment, naive T cells begin a slow proliferation that is independent of cognate antigen yet requires recognition of major histocompatibility complex-bound self-peptides. We have followed the phenotypic and functional changes that occur when naive CD8(+) T cells undergo this type of expansion in a lymphopenic environment. Naive T cells undergoing homeostasis-driven proliferation convert to a phenotypic and functional state similar to that of memory T cells, yet distinct from antigen-activated effector T cells. Naive T cells dividing in a lymphopenic host upregulate CD44, CD122 (interleukin 2 receptor beta) and Ly6C expression, acquire the ability to rapidly secrete interferon gamma, and become cytotoxic effectors when stimulated with cognate antigen. The conversion of naive T cells to cells masquerading as memory cells in response to a homeostatic signal does not represent an irreversible differentiation. Once the cellularity of the lymphoid compartment is restored and the T cells cease their division, they regain the functional and phenotypic characteristics of naive T cells. Thus, homeostasis-driven proliferation provides a thymus-independent mechanism for restoration of the naive compartment after a loss of T cells. |
Databáze: |
MEDLINE |
Externí odkaz: |
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