Abstract
IL-2 is crucial to T cell homeostasis, especially of CD4(+) T regulatory cells and memory CD8(+) cells, as evidenced by vigorous proliferation of these cells in vivo following injections of superagonist IL-2/anti-IL-2 antibody complexes. The mechanism of IL-2/anti-IL-2 antibody complexes is unknown owing to a lack of understanding of IL-2 homeostasis. We show that IL-2 receptor alpha (CD25) plays a crucial role in IL-2 homeostasis. Thus, prolongation of IL-2 half-life and blocking of CD25 using antibodies or CD25-deficient mice led in combination, but not alone, to vigorous IL-2-mediated T cell proliferation, similar to IL-2/anti-IL-2 antibody complexes. These data suggest an unpredicted role for CD25 in IL-2 homeostasis.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Antibodies, Blocking / administration & dosage
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Antigen-Antibody Complex / metabolism*
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Half-Life
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Homeostasis
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Immunoglobulin G / metabolism
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Interleukin-2 / immunology*
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Interleukin-2 / metabolism*
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Interleukin-2 Receptor alpha Subunit / antagonists & inhibitors
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Interleukin-2 Receptor alpha Subunit / deficiency
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Interleukin-2 Receptor alpha Subunit / genetics
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Interleukin-2 Receptor alpha Subunit / metabolism*
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Mice
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Mice, Congenic
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Mice, Inbred C57BL
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Mice, Knockout
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Mice, Transgenic
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Receptors, Fc / metabolism
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Recombinant Fusion Proteins / immunology
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Recombinant Fusion Proteins / metabolism
Substances
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Antibodies, Blocking
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Antigen-Antibody Complex
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Il2ra protein, mouse
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Immunoglobulin G
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Interleukin-2
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Interleukin-2 Receptor alpha Subunit
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Receptors, Fc
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Recombinant Fusion Proteins