English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Plus monthly

Global: Zendy Tools annual

Global: Zendy Tools monthly

Global: Zendy Free Plan

Full activation of TH1 helper T lymphocytes requires ligation of the specific T-cell antigen receptor (TCR) and a second signal provided by costimulator molecule(s) expressed on particular antigen-presenting cells. Stimulation via the TCR complex alone generates a subsequent unresponsive state characterized by an inability to produce interleukin 2. We report here that such anergic cells exhibit multiple alterations in TCR-associated signaling. The basal levels of intracellular free calcium and phosphatidylinositol 1,4,5-trisphosphate are elevated in anergic cells, and the levels fail to increase significantly upon subsequent restimulation. Examination of phospholipase C-gamma 1 reveals evidence for post-translational modification, correlating with increased tyrosine phosphorylation of the molecule. Tyrosine phosphorylation of additional substrates identified from whole-cell lysates also is altered compared to untreated cells, suggesting a modification in net tyrosine kinase activity. Although the level of kinase activity present in TCR/CD3 or Lck immunoprecipitates is modestly altered after induction of anergy, there is a dramatic increase in specific Fyn-associated tyrosine kinase activity in anergic cells and increased phosphorylation of a 110-kDa protein that is coimmunoprecipitated with Fyn. These results are consistent with a model in which anergic TH1 lymphocytes display a fundamental alteration in TCR-mediated tyrosine kinase activity, associated with changes in phospholipase C-gamma 1, inositol phosphates, and intracellular free calcium.

Anergic T-lymphocyte clones have altered inositol phosphate, calcium, and tyrosine kinase signaling pathways.