The Actin-Capping Protein Alpha-Adducin Is Required for T-Cell Costimulation

Thauland, Timothy J.; Khan, Humza A.; Butte, Manish J.

doi:10.3389/fimmu.2019.02706

Cited by 4 publications

(3 citation statements)

References 23 publications

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“…The co-stimulation signal through CD28 was completely eliminated without ADD1, suggesting the role of actin-capping in T cells. ADD1 is also necessary for the complete activation of CD4 + T cells in response to antigens using a conditional knockout model ( Thauland et al, 2019 ). In this study, the high score group with an immune activation environment enriched high levels of effector cells, probably due to the high expression levels of ADD1, in which CD28-mediated co-stimulation results in T-cell activation.…”

Section: Discussionmentioning

confidence: 99%

A tumor-associated endothelial signature score model in immunotherapy and prognosis across pan-cancers

Chen,

Zhang,

Huang

et al. 2023

Front. Pharmacol.

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Background: The tumor-associated endothelial cell (TAE) component plays a vital role in tumor immunity. However, systematic tumor-associated endothelial-related gene assessment models for predicting cancer immunotherapy (CIT) responses and survival across human cancers have not been explored. Herein, we investigated a TAE gene risk model to predict CIT responses and patient survival in a pan-cancer analysis.Methods: We analyzed publicly available datasets of tumor samples with gene expression and clinical information, including gastric cancer, metastatic urothelial cancer, metastatic melanoma, non-small cell lung cancer, primary bladder cancer, and renal cell carcinoma. We further established a binary classification model to predict CIT responses using the least absolute shrinkage and selection operator (LASSO) computational algorithm.Results: The model demonstrated a high predictive accuracy in both training and validation cohorts. The response rate of the high score group to immunotherapy in the training cohort was significantly higher than that of the low score group, with CIT response rates of 51% and 27%, respectively. The survival analysis showed that the prognosis of the high score group was significantly better than that of the low score group (all p < 0·001). Tumor-associated endothelial gene signature scores positively correlated with immune checkpoint genes, suggesting that immune checkpoint inhibitors may benefit patients in the high score group. The analysis of TAE scores across 33 human cancers revealed that the TAE model could reflect immune cell infiltration and predict the survival of cancer patients.Conclusion: The TAE signature model could represent a CIT response prediction model with a prognostic value in multiple cancer types.

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Section: Discussionmentioning

confidence: 99%

A tumor-associated endothelial signature score model in immunotherapy and prognosis across pan-cancers

Chen,

Zhang,

Huang

et al. 2023

Front. Pharmacol.

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“…By assembling the spectrin–actin network, ADD1 physically supports the plasma membrane, also mediating signal transduction in different cellular pathways ( Kiang and Leung, 2018 ). The role of ADD1 in the CD4+ and CD8+ T-cell activation and co-stimulation of CD28 has been recently evidenced ( Thauland et al., 2019 ), suggesting that A. pegreffii in the naïve rat could stimulate differentiation of both killer and helper T cells. Differentiation toward the T killer cells is further supported by a high expression of the T-cell surface glycoprotein CD8 alpha chain precursor gene, which primarily serves as a co-receptor for the MHC class I molecule:peptide complex on cytotoxic cells.…”

Section: Discussionmentioning

confidence: 99%

Rat and fish peripheral blood leukocytes respond distinctively to Anisakis pegreffii (Nematoda, Anisakidae) crude extract

Hrabar

Petrić

Cavallero³

et al. 2022

Front. Cell. Infect. Microbiol.

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Infective third-stage larvae (L3) of the marine nematode Anisakis pegreffii cause inflammation and clinical symptoms in humans, their accidental host, that subside and self-resolve in a couple of weeks after L3 die. To characterise the differences in an early immune response of a marine vs. terrestrial host, we stimulated peripheral blood leukocytes (PBLs) of fish (paratenic host) and rat (accidental, human-model host) with A. pegreffii crude extract and analysed PBL transcriptomes 1 and 12 h post-stimulation. Fish and rat PBLs differentially expressed 712 and 493 transcripts, respectively, between 1 and 12 h post-stimulation (false discovery rate, FDR <0.001, logFC >2). While there was a difference in the highest upregulated transcripts between two time-points, the same Gene Ontologies, biological processes (intracellular signal transduction, DNA-dependent transcription, and DNA-regulated regulation of transcription), and molecular functions (ATP and metal ion binding) were enriched in the two hosts, showing an incrementing dynamic between 1 and 12 h. This suggests that the two distinct hosts employ qualitatively different transcript cascades only to achieve the same effect, at least during an early innate immunity response. Activation of later immunity elements and/or a combination of other host’s intrinsic conditions may contribute to the death of L3 in the terrestrial host.

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“…Actin dynamics are largely regulated by a family of Rho GTPases, which themselves are controlled by many proteins and a diverse range of post-translational modifications that regulate subcellular localization and GTP exchange 34 – 39 . Molecules further downstream that influence actin dynamics promote the bundling of filaments 40 , the severing of filaments 41 , 42 , capping of actin 43 , branching of filaments 44 , 45 and more. Important secondary mediators of force transduction include serum response factor (SRF), its coactivator myocardin-related transcription factor A (MRTFA) and yes-associated protein (YAP) or its homologue, transcriptional co-activator with PDZ-binding motif (TAZ).…”

Section: Mechanosensing Pathwaysmentioning

confidence: 99%

Tuning immunity through tissue mechanotransduction

Bartleson

Butenko

et al. 2022

Nat Rev Immunol

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Immune responses are governed by signals from the tissue microenvironment, and in addition to biochemical signals, mechanical cues and forces arising from the tissue, its extracellular matrix and its constituent cells shape immune cell function. Indeed, changes in biophysical properties of tissue alter the mechanical signals experienced by cells in many disease conditions, in inflammatory states and in the context of ageing. These mechanical cues are converted into biochemical signals through the process of mechanotransduction, and multiple pathways of mechanotransduction have been identified in immune cells. Such pathways impact important cellular functions including cell activation, cytokine production, metabolism, proliferation and trafficking. Changes in tissue mechanics may also represent a new form of ‘danger signal’ that alerts the innate and adaptive immune systems to the possibility of injury or infection. Tissue mechanics can change temporally during an infection or inflammatory response, offering a novel layer of dynamic immune regulation. Here, we review the emerging field of mechanoimmunology, focusing on how mechanical cues at the scale of the tissue environment regulate immune cell behaviours to initiate, propagate and resolve the immune response.

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The Actin-Capping Protein Alpha-Adducin Is Required for T-Cell Costimulation

Cited by 4 publications

References 23 publications

A tumor-associated endothelial signature score model in immunotherapy and prognosis across pan-cancers

A tumor-associated endothelial signature score model in immunotherapy and prognosis across pan-cancers

Rat and fish peripheral blood leukocytes respond distinctively to Anisakis pegreffii (Nematoda, Anisakidae) crude extract

Tuning immunity through tissue mechanotransduction

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