ArticleCell stress & chaperones2008
Protein kinase C signaling during T cell activation induces the endoplasmic reticulum stress response.
Article in Cell stress & chaperones, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 37 citations in OpenAlex.
- TMED inhibition suppresses cell surface PD-1 expression and overcomes T cell dysfunction.Journal for immunotherapy of cancer · 2024Article
- TMED4 facilitates regulatory T cell suppressive function via ROS homeostasis in tumor and autoimmune mouse models.The Journal of clinical investigation · 2024Article
- Navigating the landscape of the unfolded protein response in CD8Frontiers in immunology · 2024Review
- Control of immune cell function by the unfolded protein response.Nature reviews. Immunology · 2023Review
- HIV-1-induced nuclear invaginations mediated by VAP-A, ORP3, and Rab7 complex explain infection of activated T cells.Nature communications · 2023Article
- HIV-Host Cell Interactions.Cells · 2023Review
- The Adaptation Model of Immunity: Signal IV Matters Most in Determining the Functional Outcomes of Immune Responses.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- The adaptation model of immunity: Is the goal of central tolerance to eliminate defective T cells or self-reactive T cells?Scandinavian journal of immunology · 2022Article
- Activation of the Unfolded Protein Response Pathway in Cytotoxic T Cells: A Comparison BetweenThe Yale journal of biology and medicine · 2019Review
- Stressed: The Unfolded Protein Response in T Cell Development, Activation, and Function.International journal of molecular sciences · 2019Review
- STING-mediated disruption of calcium homeostasis chronically activates ER stress and primes T cell death.The Journal of experimental medicine · 2019Article
- ER stress-induced mediator C/EBP homologous protein thwarts effector T cell activity in tumors through T-bet repression.Nature communications · 2019Article
- Stabilization of cytokine mRNAs in iNKT cells requires the serine-threonine kinase IRE1alpha.Nature communications · 2018Article
- Correlation of increased Th17/Treg cell ratio with endoplasmic reticulum stress in chronic kidney disease.Medicine · 2018Article
- Palmitate inhibits arthritis by inducing t-bet and gata-3 mRNA degradation in iNKT cells via IRE1α-dependent decay.Scientific reports · 2017Article
- Endoplasmic reticulum stress regulates tumor growth and anti-tumor immunity: a promising opportunity for cancer immunotherapy.Cancer immunology, immunotherapy : CII · 2017Review
- Role of endoplasmic reticulum stress in rheumatoid arthritis pathogenesis.Journal of Korean medical science · 2014Review
- The serine-threonine kinase inositol-requiring enzyme 1α (IRE1α) promotes IL-4 production in T helper cells.The Journal of biological chemistry · 2013Article
- Endoplasmic reticulum stress regulates the innate immunity critical transcription factor IRF3.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Wogonin ameliorates lipotoxicity-induced apoptosis of cultured vascular smooth muscle cells via interfering with DAG-PKC pathway.Acta pharmacologica Sinica · 2011Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
T cell receptor (TCR) ligation (signal one) in the presence of co-stimulation (signal two) results in downstream signals that increase protein production enabling naïve T cells to fully activate and gain effector function. Enhanced production of proteins by a cell requires an increase in endoplasmic reticulum (ER) chaperone expression, which is accomplished through activation of a cellular mechanism known as the ER stress response. The ER stress response is initiated during the cascade of events that occur for the activation of many cells; however, this process has not been comprehensively studied for T cell function. In this study, we used primary T cells and mice circulating TCR transgenic CD8(+) T cells to investigate ER chaperone expression in which TCR signaling was initiated in the presence or absence of co-stimulation. In the presence of both signals, in vitro and in vivo analyses demonstrated induction of the ER stress response, as evidenced by elevated expression of GRP78 and other ER chaperones. Unexpectedly, ER chaperones were also increased in T cells exposed only to signal one, a treatment known to cause T cells to enter the 'nonresponsive' states of anergy and tolerance. Treatment of T cells with an inhibitor to protein kinase C (PKC), a serine/threonine protein kinase found downstream of TCR signaling, indicated PKC is involved in the induction of the ER stress response during the T cell activation process, thus revealing a previously unknown role for this signaling protein in T cells. Collectively, these data suggest that induction of the ER stress response through PKC signaling is an important component for the preparation of a T cell response to antigen.
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