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© Andres Alcover
Scanning electron microscopy showing a conjugate formed between a T lymphocyte and an antigen presenting cell. It is worth noting the long shape of the T cell (Tc) polarized towards the antigen presenting cell (APC) and the membrane protrusions that adhere the T lymphocyte to the antigen presenting cell.
Publication : The Journal of biological chemistry

Triggering of T-lymphocytes via either T3-Ti or T11 surface structures opens a voltage-insensitive plasma membrane calcium-permeable channel: requirement for interleukin-2 gene function

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in The Journal of biological chemistry - 15 Jan 1989

Gardner P, Alcover A, Kuno M, Moingeon P, Weyand CM, Goronzy J, Reinherz EL

Link to Pubmed [PMID] – 2562953

J. Biol. Chem. 1989 Jan;264(2):1068-76

Stimulation of human T-lymphocytes via either the surface T3-Ti antigen-major histocompatibility complex receptor complex or the T11 molecule results in clonal proliferation through a calcium-dependent mechanism. To investigate this signal transduction, plasma membrane calcium-permeable channels were characterized in T-lymphocytes by means of whole cell or single channel patch-clamp recordings. Stimulation of T-lymphocytes via either structure results in opening of an identical set of voltage-insensitive plasma membrane Ca2+-permeable channels through the action of a diffusible second messenger. Previous work with excised inside-out patches suggests that inositol 1,4,5-trisphosphate is the activating second messenger of the voltage-insensitive T-cell Ca2+-permeable channel. Since there is a significant increase in phosphoinositide turnover after stimulation via either the T3-Ti or T11 pathway, it is suggested that triggering of either structure opens a common set of channels through this mechanism. Furthermore, currents flowing through Ca2+-permeable channels are apparently autoregulated, as inward conductance is abolished by elevation of Ca2+ concentration in the bathing solution. In particular, the steady-state rise in interleukin-2 (T-cell growth factor) mRNA is dependent on the rise of [Ca2+]i resulting from ion movement across this channel.

https://www.ncbi.nlm.nih.gov/pubmed/2562953