#Tcell-mediated
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castltrastondrs.medsky.network
VZV latency is mainly controlled by VZV-specific #Tcell-mediated immunity and when this immune response declines, because of aging or iatrogenic immunosuppression,
October 30, 2026 at 6:28 AM
jlbjournal.bsky.social
Jia Hong & Su Shao identify a #SOX2-#TSTA3 axis involved in suppressing CD8+ #Tcell mediated antitumor immune responses in #BreastCancer by promoting #Fucosylation of #PDL1
SOX2/TSTA3 suppresses CD8+ T-cell-mediated immune response in breast cancer by regulating programmed death ligand-1 fucosylation
In breast cancer cells, SOX2 transcriptionally activates TSTA3 expression. Elevated TSTA3 enhances programmed death ligand-1 fucosylation, which increases
doi.org
October 30, 2026 at 7:17 PM
castltrastondrs.medsky.network
Importantly, there is limited information on whether #Tcell -mediated #immunity composed by mCD4+ T helper cells and mCD8+ T cells, known for their capacity to kill virally infected cells, is preserved during aging, especially in end-of-life patients…
April 4, 2025 at 12:36 PM
castltrastondrs.medsky.network
The understanding the infection & vaccine-mediated humoral, #Bcell & #Tcell responses, the durability of the immune responses & how variants continue to threaten the efficacy of #Covid19vaccines.

www.sciencedirect.com/science/arti...

www.cell.com/iscience/ful...
Durability of immune responses to SARS-CoV-2 infection and vaccination
Infection with SARS-CoV-2 in humans has caused a pandemic of unprecedented dimensions. SARS-CoV-2 is primarily transmitted through respiratory droplet…
www.sciencedirect.com
January 28, 2025 at 7:36 AM
castltrastondrs.medsky.network
#MedSky🧪 #ImmunoSky summarize the impacts of nutrients and associated factors (e.g., nutrient-derived metabolic intermediates and extracellular metabolites) on #Tcell activation, differentiation & function & the underlying mechanisms
rupress.org/jem/article/...
Signal 4 nutrients in directing T cell activation. (A) Overview of Signals 1 (TCR binding to antigen presented on MHC molecules), 2 (co-stimulation by CD28), 3 (cytokine signals), and 4 (nutrients) that drive T cell immunity. Signal 4 is mediated through a three-tiered process composed of nutrient transport, sensing, and signal transduction. Signals 1–3 can augment Signal 4 by promoting the expression of nutrient transporters, while Signal 4 also interplays with Signals 1–3, for example, by shaping signaling and metabolic events. Integration of Signals 1–4 results in metabolic reprogramming, associated with increased mTORC1 signaling, c-MYC activity, and activation of biosynthesis pathways and cellular bioenergetics, altogether driving T cell activation. (B) Glucose and amino acid uptake into T cells, mediated by membrane transporters, promotes mTORC1 activation and metabolic reprogramming. Sestrins, CASTOR1, and SAMTOR represent cytosolic sensors of amino acids. Leucine and arginine respectively bind to and sequester Sestrins and CASTOR1 from GATOR2, relieving their suppressive effects on GATOR2, thereby allowing GATOR2 to promote mTORC1 activation (via inhibiting GATOR1). SAMTOR senses the methionine metabolite S-adenosylmethionine (SAM). SAM binding to SAMTOR disrupts SAMTOR–GATOR1 complex formation, thereby inhibiting the ability of GATOR1 to negatively regulate mTORC1 activation. SLC38A9 senses arginine in the lysosome, and both SLC38A9 and v-ATPase signal the increase in intralysosomal amino acid concentrations to promote mTORC1 activation, which may involve controlling the efflux of amino acids from the lysosome. Arginine also promotes mTORC1 signaling by regulating TSC–RHEB signaling. Glutamine signals through ADP ribosylation factor 1 (ARF-1) to promote mTORC1. Asparagine is sensed by LCK to promote TCR-mediated PI3K–Akt signaling. The SWI/SNF complex (including SMARCB1) inhibits gene expression of Castor1 and thereby enhances mTORC1 activity. CCDC101-assoc…
November 20, 2024 at 4:26 PM
castltrastondrs.medsky.network
#MedSky🧪#IDSky Durable #Tcell responses to #SARSCoV2 antigens after infection or vaccination improve immune-mediated #viralclearance. To date, population-based surveys of #COVID19 #adaptiveimmunity have focused on testing for IgG antibodies that bind spike protein and/or neutralize the virus.
Inforgraphic
May 6, 2024 at 8:55 AM
I am delighted to share the latest article from our lab at Infinity (Toulouse, France) in which we identify HP1 variants as rheostats that finely tune the balance between tolerance and immunity.

#Immunology #Tcell #Treg #Immunotherapy

www.nature.com/articles/s41...
Heterochromatic gene silencing controls CD4+ T cell susceptibility to regulatory T cell-mediated suppression in a murine allograft model - Nature Communications
Regulatory T cells play critical roles in the control and modulation of immune responses. Here the authors implicate heterochromatic gene silencing in the susceptibility of CD4+ T cell to regulatory T...
www.nature.com
January 13, 2025 at 12:13 PM
immunoeditor.bsky.social
The September issue of #Science #Immunology is out! This week: METTL1 m⁷G RNA modification of NAD+ #metabolism → #macrophage -mediated #inflammation; proenkaphalin+ #Tregs restrain skin inflamm via control of #nociception; #RNA helicase DDX55 is regulator of naïve #TCell homeostasis

scim.ag/3HKC5DP
Shining a Light on Naïve T Cell Homeostasis: Homeostatic maintenance of naïve T cells is critical to maintain a large and diverse T cell pool. However, the underlying mechanisms regulating this process are not well understood. Wu et al. report that the RNA helicase DDX55 regulates the homeostatic maintenance of naïve T cells by preventing MYC from binding to enhancer- and promoter-like transposable elements (TEs) near T cell activation genes. In naïve T cells, DDX55 prevents the inappropriate activation of TEs and ensures their genomic stability by preventing R-loop formation. This month’s cover features a light bulb with its filament stylized as a DNA double helix. Its left half glows with an intact filament, symbolizing TEs as regulators, and its right side is dimmed and features a broken filament, representing TEs’ disruptive potential. Credit: Bingyu Yang and Jianling Zhu/Sichuan University
September 5, 2025 at 6:23 PM
zimmorn.bsky.social
🔓 New #CellPreview by Prof. Kai W. Wucherpfennig @harvard.edu highlights our work on LAG3!

Key take:
• Cbl-mediated, non-degradative poly-ubiquitination at K498 unlocks LAG3 signaling
• Marks TILs that respond to PD-1/LAG3 combo

#LAG3 #Immunotherapy #PD1 #TCell
www.cell.com/cell/fulltex...
Unlocking LAG3: Ubiquitin’s unexpected role
The inhibitory receptor LAG3 is the target of the FDA-approved mAb relatlimab, but its mechanism of signaling is not well understood. In this issue of Cell, Jiang et al. demonstrate that ubiquitinatio...
www.cell.com
May 2, 2025 at 2:08 AM
immunologypodcast.com
In this @natimmunol.nature.com paper, researchers in the lab of Dr. Mahnoor Gondal at @umich.edu have uncovered a previously unrecognized role for MHC class I in modulating CD4+ #TCell-mediated immunity.

📄: https://go.nature.com/4uRXpuH
🎧: https://bit.ly/4e1qwWh
April 8, 2026 at 5:25 PM
newsmedical.bsky.social
Cancer cells block T-cell activation, but new therapies restore immune defenses 🧬🛡️✨ www.news-medical.net/news/2024120... #CancerResearch #Immunotherapy #TCell #Tumor #MonocyteScience #Oncology #ImmuneResistance #PrecisionMedicine #Cancer @natureportfolio.bsky.social
Cancer cells block T-cell activation, but new therapies restore immune defenses
Cancer cells impair monocyte-mediated T-cell activation by disrupting inflammatory pathways in the tumor microenvironment. Restoring balance through PGE2 inhibition and IFN-I enhancement could renew i...
www.news-medical.net
December 4, 2024 at 10:42 PM
plosbiology.org
CD8+ T cells can target & eliminate malignant #tumor cells, but tumors can develop resistance mechanisms to escape them. This study shows that loss of the E3 #ubiquitin ligase CUL5 enhances CD8+ #Tcell #cytotoxicity & anti PD-1 efficacy by inhibiting #autophagy @plosbiology.org 🧪 plos.io/3Mv1EuR
Model describing the effect of CUL5 on the sensitivity of bladder cancer cells to CD8+ T cell-mediated killing. CUL5-KO could reduce the ubiquitination of PTBP1, thereby increasing the alternative splicing of RUBCN pre-mRNA, leading to an increase in Rubicon-S which inhibits autophagy, and thus enhances the sensitivity of bladder cancer cells to CD8+ T cell-mediated killing (cartoon created in BioRender).
February 11, 2026 at 8:55 AM
plosbiology.org
CD8+ T cells can target & eliminate malignant #tumor cells, but tumors can develop resistance mechanisms to escape them. This study shows that loss of the E3 #ubiquitin ligase CUL5 enhances CD8+ #Tcell #cytotoxicity & anti PD-1 efficacy by inhibiting #autophagy @plosbiology.org 🧪 plos.io/3Mv1EuR
Model describing the effect of CUL5 on the sensitivity of bladder cancer cells to CD8+ T cell-mediated killing. CUL5-KO could reduce the ubiquitination of PTBP1, thereby increasing the alternative splicing of RUBCN pre-mRNA, leading to an increase in Rubicon-S which inhibits autophagy, and thus enhances the sensitivity of bladder cancer cells to CD8+ T cell-mediated killing (cartoon created in BioRender).
February 10, 2026 at 5:25 PM
plosbiology.org
CD8+ T cells can target & eliminate malignant #tumor cells, but tumors can develop resistance mechanisms to escape them. This study shows that loss of the E3 #ubiquitin ligase CUL5 enhances CD8+ #Tcell #cytotoxicity & anti PD-1 efficacy by inhibiting #autophagy @plosbiology.org 🧪 plos.io/3Mv1EuR
Model describing the effect of CUL5 on the sensitivity of bladder cancer cells to CD8+ T cell-mediated killing. CUL5-KO could reduce the ubiquitination of PTBP1, thereby increasing the alternative splicing of RUBCN pre-mRNA, leading to an increase in Rubicon-S which inhibits autophagy, and thus enhances the sensitivity of bladder cancer cells to CD8+ T cell-mediated killing (cartoon created in BioRender).
February 10, 2026 at 1:55 PM
embomolmed.org
Glycans on non-structural protein 1 prevent premature #Tcell mediated #DengueVirus clearance

By F. Idris, S. Alonso & colleagues at National Centre for Infectious Diseases Singapore

🗞️ doi.org/10.1038/s443...
September 19, 2025 at 2:10 PM