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T cell activation in the absence of interleukin 2 (IL 2) results in the induction of high‐affinity IL 2 receptor unable to transmit a proliferative signal
Author(s) -
Proust Jacques J.,
Shaper Nancy L.,
Buchholz Meredith A.,
Nordin Albert A.
Publication year - 1991
Publication title -
european journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.272
H-Index - 201
eISSN - 1521-4141
pISSN - 0014-2980
DOI - 10.1002/eji.1830210214
Subject(s) - biology , interleukin 2 , extracellular , intracellular , receptor , microbiology and biotechnology , t cell , recombinant dna , biochemistry , immunology , immune system , gene
Abstract Although interleukin 2 (IL2) clearly up‐regulates the expression of the p55 chain of the IL 2 receptor (IL 2R) little is known about its role in the induction of the high‐affinity IL 2R. Resting T lymphocytes were induced to express IL 2R under experimental conditions in which IL 2 production was not induced or was prevented. Under these conditions high‐ and low‐affinity IL 2R were easily demonstrated by Scatchard analysis. Northern blot analysis confirmed the accumulation of p55 specific mRNA and the absence of the IL 2 transcript. High‐affinity IL 2R induced in the complete absence of IL 2 were unable to transmit a proliferative response unless exposed to extremely high concentrations of IL 2. The addition of picomolar amounts of recombinant IL 2 or the initiation of endogenous IL 2 production during the induction period restored the functionality of high‐affinity IL 2R. Also, T cells induced to generate IL 2 displayed functional high‐affinity IL 2R even in the presence of monoclonal antibodies blocking extracellular IL 2 and IL 2R. These results indicate that the presence of IL 2 during the early phase of T cell activation is an absolute requirement for the induction of fully operational high‐affinity IL 2R and that low amounts of intracellular IL 2 are sufficient to confer functional properties to these receptors. The data also suggest that an intracellular as well as an extracellular high‐affinity structure, expressed as a consequence of cell activation, is responsible for conferring competence to the high‐affinity IL 2R involved in IL 2‐dependent proliferation.