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APC activation by IFN-alpha decreases regulatory T cell and enhances Th cell functions
- Source :
- Journal of immunology (Baltimore, Md. : 1950). 184(11)
- Publication Year :
- 2010
-
Abstract
- Type I IFNs are central to a vast array of immunological functions. Their early induction in innate immune responses provides one of the most important priming mechanisms for the subsequent establishment of adaptive immunity. The outcome is either promotion or inhibition of these responses, but the conditions under which one or the other prevails remain to be defined. The main objective of the current study was to determine the involvement of IFN-α on murine CD4+CD25− Th cell activation, as well as to define the role played by this cytokine on CD4+CD25+ regulatory T (Treg) cell proliferation and function. Although IFN-α promotes CD4+CD25− Th cells coincubated with APCs to produce large amounts of IL-2, the ability of these cells to respond to IL-2 proliferative effects is prevented. Moreover, in medium supplemented with IFN-α, IL-2–induced CD4+CD25+ Treg cell proliferation is inhibited. Notably, IFN-α also leads to a decrease of the CD4+CD25+ Treg cell suppressive activity. Altogether, these findings indicate that through a direct effect on APC activation and by affecting CD4+CD25+ Treg cell-mediated suppression, IFN-α sustains and drives CD4+CD25− Th cell activation.
- Subjects :
- Regulatory T cell
medicine.medical_treatment
Immunology
Blotting, Western
Priming (immunology)
Antigen-Presenting Cells
chemical and pharmacologic phenomena
Cell Separation
Receptor, Interferon alpha-beta
Biology
Lymphocyte Activation
T-Lymphocytes, Regulatory
Mice
medicine
Immunology and Allergy
Animals
IL-2 receptor
Cells, Cultured
Cell Proliferation
Innate immune system
Cell growth
Interferon-alpha
hemic and immune systems
T-Lymphocytes, Helper-Inducer
Acquired immune system
Flow Cytometry
Coculture Techniques
Cell biology
Mice, Inbred C57BL
Cytokine
medicine.anatomical_structure
Interleukin-2
Female
Cell activation
Subjects
Details
- ISSN :
- 15506606
- Volume :
- 184
- Issue :
- 11
- Database :
- OpenAIRE
- Journal :
- Journal of immunology (Baltimore, Md. : 1950)
- Accession number :
- edsair.doi.dedup.....6783ce2d867ec42da03bacfd297b3265