IL-2/anti-IL-2 antibody complexes show strong biological activity by avoiding interaction with IL-2 receptor alpha subunit CD25.
Details
Serval ID
serval:BIB_72BA2B267468
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
IL-2/anti-IL-2 antibody complexes show strong biological activity by avoiding interaction with IL-2 receptor alpha subunit CD25.
Journal
Proceedings of the National Academy of Sciences of the United States of America
ISSN
1091-6490 (Electronic)
ISSN-L
0027-8424
Publication state
Published
Issued date
2010
Volume
107
Number
5
Pages
2171-2176
Language
english
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Publication Status: ppublish
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.
Keywords
Animals, Antibodies, Blocking/administration & dosage, Antigen-Antibody Complex/metabolism, Half-Life, Homeostasis, Immunoglobulin G/metabolism, Interleukin-2/immunology, Interleukin-2/metabolism, Interleukin-2 Receptor alpha Subunit/antagonists & inhibitors, Interleukin-2 Receptor alpha Subunit/deficiency, Mice, Mice, Congenic, Mice, Inbred C57BL, Mice, Knockout, Mice, Transgenic, Receptors, Fc/metabolism, Recombinant Fusion Proteins/immunology, Recombinant Fusion Proteins/metabolism
Pubmed
Web of science
Open Access
Yes
Create date
23/02/2010 15:58
Last modification date
20/08/2019 15:30