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Induction of the interleukin-2 receptor (p55) by interferons
M Onji1, S Yamaguchi, T Masumoto
1Third Department of Internal Medicine, Ehime University School of Medicine, Japan.
Insights
Human interferons (IFN) increase interleukin-2 receptor (IL-2R) expression on immune cells. This study shows IFN-alpha, -beta, and -gamma boost soluble IL-2R levels and mRNA in mononuclear cells, indicating a role in immune regulation.
Area of Science:
- Immunology
- Molecular Biology
Background:
- Interferons (IFN) are crucial cytokines in immune response regulation.
- Interleukin-2 receptor (IL-2R) expression is a marker of lymphocyte activation.
Purpose of the Study:
- To investigate the effect of human interferons (IFN) on interleukin-2 receptor (IL-2R) expression in peripheral blood mononuclear cells (PBMCs).
- To assess the role of IFN in immune response modulation through IL-2R induction.
Main Methods:
- Enzyme-linked immunosorbent assay (ELISA) to measure soluble IL-2R (sIL-2R) levels in vitro and in vivo.
- Dual flow cytometry to analyze IL-2R expression on specific immune cell subsets.
- Northern blot analysis to quantify IL-2R-specific mRNA levels.
Main Results:
- Serum sIL-2R levels significantly increased in chronic hepatitis B patients receiving IFN-alpha or IFN-beta therapy.
- In vitro culture with IFN-alpha, -beta, or -gamma led to significant increases in supernatant sIL-2R levels.
- IFN-alpha treatment induced IL-2R expression on CD4+ T cells and CD20+ B cells, with increased IL-2R mRNA.
Conclusions:
- Human interferons, particularly IFN-alpha, induce IL-2R expression on PBMCs, including T cells and B cells.
- IFN-alpha stimulation leads to increased IL-2R mRNA, suggesting transcriptional regulation.
- These findings highlight IFN's role in modulating immune responses via IL-2R induction and lymphocyte activation.
Abstract:
The effect of human interferon (IFN) on the interleukin-2 receptor (IL-2R, p55) expression by peripheral blood mononuclear cells was investigated both in vitro and in vivo. IL-2R induction was assessed by the soluble IL-2R level in vitro and in vivo, which was measured by ELISA using two monoclonal antibodies to IL-2R(p55). Serum levels of sIL-2R increased significantly during IFN-alpha or IFN-beta therapy in 13 patients with chronic hepatitis B. When mononuclear cells were cultured with IFNs-alpha, -beta, or -gamma, the sIL-2R levels in the supernatant increased significantly. Dual flow cytometric analysis demonstrated that IL-2R was expressed on CD4+ and CD20+ mononuclear cells treated with IFN-alpha in vitro. CD4+ T cells and B cells may release sIL-2R when these cells are stimulated with IFN-alpha. RNA isolated from mononuclear cells treated with IFN-alpha contained increased levels of IL-2R-specific mRNA, as indicated by Northern blot analysis using an IL-2R-specific mRNA probe. These findings help to indicate how IFN plays a role in the regulation of the immune response, because IL-2R induction is known to be associated with lymphocyte activation.