期刊
JOURNAL OF IMMUNOLOGY
卷 174, 期 6, 页码 3158-3163出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.174.6.3158
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资金
- NIAID NIH HHS [AI45809, AI41079, AI37108, AI07244] Funding Source: Medline
- NIA NIH HHS [AG20186] Funding Source: Medline
Homeostatic proliferation of naive T cells transferred to T cell-deficient syngeneic mice is driven by low-affinity self MHC/peptide ligands and the cytokine IL-7. In addition to homeostatic proliferation, a subset of naive T cells undergoes massive proliferation in chronically immunodeficient hosts, but not in irradiated normal hosts. Such rapid T cell proliferation occurs largely independent of homeostatic factors, because it was apparent in the absence of IL-7 and in T cell-sufficient hosts devoid of functional T cell immunity. Strikingly, immunodeficient mice raised under germfree conditions supported only slow homeostatic proliferation, but not the marked T cell proliferation observed in conventionally raised immunodeficient mice. Thus, polyclonal naive T cell expansion in T cell deficient hosts can be driven predominantly by either self-Ags or foreign Ags depending on the host's previous state of T cell immunocompetency.
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