In:
The Journal of Immunology, The American Association of Immunologists, Vol. 184, No. 6 ( 2010-03-15), p. 2855-2862
Abstract:
IFN-γ regulates multiple processes in the immune system. Although its antimicrobial effector functions are well described, less is known about the mechanisms by which IFN-γ regulates CD8+ T cell homeostasis. With the help of adoptive T cell transfers, we show in this study that IFN-γR signaling in CD8+ T cells is dispensable for expansion, contraction, and memory differentiation in response to peptide vaccination. In contrast, host IFN-γR signaling counterregulates CD8+ T cell responses and the generation of effector memory T cell processes, which are partially regulated by CD11b+ cells. Similar to vaccination-induced proliferation, host IFN-γR signaling limits the expansion of naive CD8+ T cells and their differentiation into effector memory-like T cells in lymphopenic mice. In contrast to peptide vaccination, IFN-γR signaling in CD8+ T cells contributes to memory fate decision in response to lymphopenia, an effect that is fully reversed by high-affinity TCR ligands. In conclusion, we show that host IFN-γR signaling controls the magnitude of CD8+ T cell responses and subsequent memory differentiation under lymphopenic and nonlymphopenic conditions. In contrast, IFN-γR signaling in CD8+ T cells does not affect cell numbers under either condition, but it directs memory fate decision in response to weak TCR ligands.
Type of Medium:
Online Resource
ISSN:
0022-1767
,
1550-6606
DOI:
10.4049/jimmunol.0902708
Language:
English
Publisher:
The American Association of Immunologists
Publication Date:
2010
detail.hit.zdb_id:
1475085-5
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