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IL-2 Signaling Pathways

Click on the “Effects” button shown in the Explore Pathways box below to reveal the primary biological effects of IL-2 signaling in different immune cell types. Click on one of the other cytokines shown in the Explore Pathways box below for information on a different common cytokine receptor gamma-chain family member.

IL-2 Signaling Pathways
Common gamma chain
Common gamma chain
IL-2
IL-2
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IL-2 R alpha
IL-2 R alpha
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IL-2/IL-15 R beta
IL-2/IL-15 R beta
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Jak1
Jak1
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Jak3
Jak3
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STAT1
STAT1
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STAT3
STAT3
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STAT5
STAT5
STAT Dimer
STAT Dimer

IL-2 Receptor-Expressing Cells:
T cells, B cells, natural killer cells,
monocytes, macrophages

IL-2 Receptor-Expressing Cells:
T cells, B cells, natural killer cells,
monocytes, macrophages

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PI 3-K
PI 3-K
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PDK-1
PDK-1
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Akt/PKB
Akt/PKB
p70 S6K
p70 S6K
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Bad
Bad
Bad
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Bad
GSK-3
GSK-3
Forkhead
Forkhead
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IRS
IRS
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Shc
Shc
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GRB2
GRB2
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SOS
SOS
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Ras
Ras
Ras
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Ras
Raf
Raf
MEK1/2
MEK1/2
ERK1/2
ERK1/2
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PIP2
PIP2
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PIP3
PIP3
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Anti-Apoptotic

Anti-Apoptotic

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Mitogenic

Mitogenic

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Target Genes
Target Genes
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IL-2 Signaling Pathways

 

Overview of IL-2 Signaling Pathways

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 be required for B cell proliferation and immunoglobulin production.

To learn more, please visit our Common gamma Chain Receptor Family Research Area.

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