IL-2 Signaling Pathways and their Primary Biological Effects in Different Immune Cell Types
Click on one of the links shown in the Explore Pathways box below to see either either the IL-2 signaling pathways or information related to one of the other common cytokine receptor gamma-chain family members.
Get Print CopyT Cell Proliferation
T Cell Proliferation
Proliferation/Survival
Proliferation/Survival
or TNF RII
or TNF RII
Cell Death
Cell Death
CD4+ T Cells
CD4+ T Cells
Activation-Induced Cell Death
Activation-Induced Cell Death
Maintenance of Peripheral
Self-Tolerance
Maintenance of Peripheral
Self-Tolerance
Development, Survival, &
Maintenance
Development, Survival, &
Maintenance
Regulatory T Cell
Development
Regulatory T Cell
Development
Maintenance
Maintenance
Effects on Regulatory T Cells
Effects on Regulatory T Cells
Memory T Cells
Memory T Cells
CD8+ T Cell
CD8+ T Cell
Division
Division
CD8+ T Cell
CD8+ T Cell
Inhibits Division
Inhibits Division
Proliferation
Proliferation
Proliferation
Proliferation
Production
Production
B Cell
B Cell
Immunoglobulin Production
Immunoglobulin Production
Overview of Primary Biological Effects of IL-2 Signaling in Different Immune Cell Types
Interleukin-2 (IL-2) is an O-glycosylated four alpha-helix bundle cytokine that is primarily produced by activated T cells, dendritic cells, and B cells. The biological activity of IL-2 is mediated by binding to a cell surface receptor complex consisting of IL-2 R alpha/CD25, IL-2/IL-15 R beta, and the common gamma-chain/IL-2 R gamma subunit. IL-2 can also bind with low affinity to IL-2 R alpha alone, or with intermediate affinity to a complex consisting of IL-2/IL-15 R beta and the common gamma-chain subunit. Functionally, IL-2 induces the expression of both IL-2 and IL-2 R alpha on activated CD4+ and CD8+ T cells and stimulates their proliferation. In contrast, IL-2 also plays an important role in the maintenance of peripheral self-tolerance both by initiating Fas-mediated activation-induced cell death of CD4+ T cells following antigen restimulation and by its ability to promote the differentiation and survival of regulatory T cells. Rather than displaying a severe immunodeficient phenotype, mice lacking IL-2, IL-2 R alpha, or IL-2 R beta accumulate activated T lymphocytes, have reduced numbers of regulatory T cells, and develop autoimmune diseases. This suggests that the maintenance of T cell homeostasis and prevention of self-reactivity is the primary function of IL-2 signaling. In addition, IL-2 may enhance the cytotoxicity of natural killer cells and may be required for B cell proliferation and immunoglobulin production.
To learn more, please visit our Common gamma Chain Receptor Family Research Area.
Get Print Copy of this Pathway
