Open AccessCostimulatory signals for human T-cell activation induce nuclear translocation of pp19/cofilin.
Author(s) -
Yvonne Samstag,
Christoph Eckerskorn,
Sebastian Wesselborg,
Stefan Henning,
Reinhard Wallich,
Stefan Meuer
Publication year - 1994
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.91.10.4494
Subject(s) - jurkat cells , microbiology and biotechnology , biology , cofilin , cd28 , t cell , t cell receptor , dephosphorylation , il 2 receptor , cytotoxic t cell , major histocompatibility complex , antigen , cell , phosphorylation , immune system , immunology , in vitro , actin cytoskeleton , cytoskeleton , biochemistry , phosphatase
Resting T lymphocytes that have recognized antigen bound to a major histocompatibility complex molecule with the T-cell receptor require costimulatory signals through accessory receptors, including CD2, CD4, CD8, and CD28, for their clonal growth and expression of their functional repertoires. Absence of costimulation, in contrast, can induce clonal anergy in vitro and selective tolerance in vivo. Here we have defined a potential intracellular messenger for T-cell activation which is strictly regulated by costimulatory signals mediated through accessory receptors: pp19/cofilin, a small actin-binding protein, undergoes dephosphorylation and subsequent translocation from the cytosol into the nucleus. In untransformed T cells this process correlates with functional responses essential for the induction of T-cell proliferation (i.e., production of interleukin 2). Moreover, spontaneous dephosphorylation as well as nuclear translocation of pp19/cofilin occur in the autonomously proliferating T-lymphoma cell line Jurkat.