NDLI: Interleukin-12 is sufficient to promote antigen-independent interferon-γ production by CD8 T cells in old mice

Content Provider	PubMed Central
Author	Rottinghaus, Erin K. Bridget, Vesosky Turner, Joanne
Copyright Year	2009
Abstract	Numerous functional defects have been identified in naive T cells from aged mice, including deficiencies in proliferation, cytokine production and signal transduction. It is well documented that the ratio of naïve to memory T cells significantly decreases with age resulting in the majority of T cells from aged hosts expressing activated/memory T-cell markers (CD44hi), yet it is unclear whether T cells with a CD44hi phenotype in aged hosts are functionally equivalent to T cells with a similar phenotype in young hosts. We have identified a population of CD44hi CD8 T cells in old mice that are capable of secreting interferon-γ (IFN-γ) in response to interleukin-12 (IL-12) stimulation. This occurred in the absence of T-cell receptor engagement, a function that was not observed in CD8 T cells from young mice. This phenotype was associated with increased IL-12 receptor β2 gene expression and IL-12 induced signal transducer and activator of transcription 4 (STAT-4) activation, even when CD8 T-cell numbers from young and old mice were normalized for CD44hi expression. Furthermore, we demonstrate that IL-12-induced STAT-4 activation was required for T helper type 1 (Th1) cytokine-induced IFN-γ production in CD8 T cells. These data illustrate that old mice possess a specialized subset of CD44hi CD8 T cells with an enhanced responsiveness to IL-12, enabling these cells to produce substantial amounts of IFN-γ in response to Th1 cytokine stimulation. We have therefore identified a functional difference in the populations of CD44hi CD8 T cells from young and old mice, and believe that understanding age-associated immunological changes is essential for helping the elderly combat deadly diseases.
Related Links	http://dx.doi.org/10.1111/j.1365-2567.2009.03061.x
Starting Page	679
File Format	PDF
ISSN	13652567
e-ISSN	13652567
Journal	Immunology
Issue Number	1 Pt 2
Volume Number	128
Language	English
Publisher	Blackwell Science Inc
Publisher Date	2009-09-01
Access Restriction	Open
Rights Holder	Blackwell Science Inc
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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