Journal
JOURNAL OF IMMUNOLOGY
Volume 166, Issue 1, Pages 232-240Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.166.1.232
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Funding
- NIAID NIH HHS [AI37326, AI35583] Funding Source: Medline
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R29AI037326, R29AI035583, R01AI037326, R01AI035583] Funding Source: NIH RePORTER
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During activation in vivo, naive CD4(+) T cells are exposed to various endogenous ligands, such as cytokines and the neurotransmitter norepinephrine (NE), To determine whether NE affects naive T cell differentiation, we used naive CD4(+) T cells sort-purified from either BALB/c or DO11.10 TCR-transgenic mouse spleens and activated these cells with either anti-CD3/anti-CD28 mAbs or APC and OVA(323-329) peptide, respectively, under Th1-promoting conditions. RT-PCR and functional assays using selective adrenergic receptor (AR) subtype antagonists showed that naive CD4+ T cells expressed only the beta (2)AR subtype to bind NE and that stimulation of this receptor generated Th1 cells that produced 2- to 4-fold more IFN-gamma, This increase was due to more IFN-gamma produced per cell upon restimulation instead of more IFN-gamma -secreting cells, as determined by IFN-gamma -specific immunofluorescence and enzyme-linked immunospot, In contrast, Th1 cell differentiation was unaffected when naive T cells were exposed to NE and activated either in the presence of a neutralizing anti-IL-12 mAb or by APC from IL-12-deficient mice. Moreover, the addition of IL-12 to the IL-la-deficient APC cultures restored the ability of NE to increase Th1 differentiation. Taken together, these results indicate that a possible link may exist between the signaling pathways used by NE and IL-12 to increase naive CD4+ T cell differentiation to a Th1 cell.
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