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Calcium-induced ERK activation in human T lymphocytes
P A Atherfold1, M S Norris, P J Robinson
1Department of Microbiology and Immunology, East Carolina University School of Medicine, Greenville, NC 27858, USA.
Molecular Immunology
|September 4, 1999
Summary
Calcium ionophores activate ERK1 and 2 in T lymphocytes, revealing a new role for calcium signaling in these cells. This rapid, dose-dependent activation is blocked by MEK inhibitors, highlighting a novel pathway.
Area of Science:
- Immunology
- Cell Signaling
- Molecular Biology
Background:
- Previous studies demonstrated calcium ionophore-induced ERK2 activation in B lymphocytes.
- The role of calcium signaling in T lymphocyte activation remained less understood.
Purpose of the Study:
- To investigate the effect of calcium ionophores on ERK1 and ERK2 activation in human primary and Jurkat T lymphocytes.
- To elucidate the signaling pathways involved in calcium-mediated T lymphocyte activation.
Main Methods:
- Stimulation of T lymphocytes with calcium ionophores (ionomycin and A23187).
- Assessing ERK1/2 activation via SDS-PAGE mobility shifts, phospho-specific antibody binding, and myelin basic protein (MBP) phosphorylation assays.
- Inhibition studies using the MEK inhibitor PD98059.
Main Results:
- Ionomycin and A23187 rapidly and transiently activated ERK1 and ERK2 in T lymphocytes in a dose-dependent manner.
- Activation was confirmed by multiple biochemical assays, including increased MBP phosphorylation.
- MEK inhibitor PD98059 blocked calcium ionophore-induced ERK1/2 activation.
Conclusions:
- Calcium fluxes play a significant role in T lymphocyte activation through the ERK1/2 pathway.
- This study identifies a novel signaling mechanism involving calcium and ERK activation in T cells.