aims at understanding #MAIT cell biology in #tissueimmunity and #cancer
passionate about #immunometabolism
based at M3 Research Center at University of Tübingen
@easlnews.bsky.social @jhepatology.bsky.social @cd1mr1.bsky.social
#Immunometabolism #MAITcells #LiverImmunology #Ferroptosis #MASLD #HCC #LipidPeroxidation #TcellDysfunction #CancerImmunotherapy #TumorMicroenvironment #FattyLiver
The PUFA–lipid peroxide axis we have identified represents a targetable metabolic checkpoint to enhance immunotherapy in HCC.
The PUFA–lipid peroxide axis we have identified represents a targetable metabolic checkpoint to enhance immunotherapy in HCC.
MASLD generates a lipid-driven immunosuppressive microenvironment by inducing metabolic exhaustion-mediated dysfunction and ferroptosis in MAIT cells - an abundant intrahepatic T cell subset with anti-tumour properties.
MASLD generates a lipid-driven immunosuppressive microenvironment by inducing metabolic exhaustion-mediated dysfunction and ferroptosis in MAIT cells - an abundant intrahepatic T cell subset with anti-tumour properties.
• Interfering with lipid peroxide formation reverses MAIT dysfunction and restores anti-cancer activity.
• A PUFA-MAIT cell gene signature correlates with poor overall survival of patients with HCC.
• Interfering with lipid peroxide formation reverses MAIT dysfunction and restores anti-cancer activity.
• A PUFA-MAIT cell gene signature correlates with poor overall survival of patients with HCC.
• PUFAs induce intracellular lipid peroxidation, driving metabolic exhaustion – i.e. mitochondrial and glycolytic dysfunction – and triggering ferroptosis.
• PUFAs induce intracellular lipid peroxidation, driving metabolic exhaustion – i.e. mitochondrial and glycolytic dysfunction – and triggering ferroptosis.
• In MASLD, MAIT cells exhibit profound functional exhaustion, including impaired cytokine production and anti-tumour activity.
• Mechanistically, PUFAs accumulate selectively in MAIT cells, not in conventional CD8⁺ or NK cells.
• In MASLD, MAIT cells exhibit profound functional exhaustion, including impaired cytokine production and anti-tumour activity.
• Mechanistically, PUFAs accumulate selectively in MAIT cells, not in conventional CD8⁺ or NK cells.
Targeting the PUFA–lipid peroxide axis represents a targetable metabolic checkpoint to enhance immunotherapy in HCC.
Targeting the PUFA–lipid peroxide axis represents a targetable metabolic checkpoint to enhance immunotherapy in HCC.
MASLD generates a lipid-driven immunosuppressive microenvironment by inducing metabolic exhaustion-mediated dysfunction and ferroptosis in MAIT cells—an abundant intrahepatic T cell subset with anti-tumour properties.
MASLD generates a lipid-driven immunosuppressive microenvironment by inducing metabolic exhaustion-mediated dysfunction and ferroptosis in MAIT cells—an abundant intrahepatic T cell subset with anti-tumour properties.
• Interfering with lipid peroxide formation reverses MAIT dysfunction and restores anti-cancer activity.
• A PUFA-MAIT cell gene signature correlates with poor overall survival of patients with HCC.
• Interfering with lipid peroxide formation reverses MAIT dysfunction and restores anti-cancer activity.
• A PUFA-MAIT cell gene signature correlates with poor overall survival of patients with HCC.
• PUFAs induce intracellular lipid peroxidation, driving metabolic exhaustion – mitochondrial and glycolytic dysfunction – and triggering ferroptosis.
• PUFAs induce intracellular lipid peroxidation, driving metabolic exhaustion – mitochondrial and glycolytic dysfunction – and triggering ferroptosis.
• In MASLD, MAIT cells exhibit profound functional exhaustion, including impaired cytokine production and anti-tumor activity.
• Mechanistically, PUFAs accumulate selectively in MAIT cells, not in conventional CD8⁺ or NK cells.
• In MASLD, MAIT cells exhibit profound functional exhaustion, including impaired cytokine production and anti-tumor activity.
• Mechanistically, PUFAs accumulate selectively in MAIT cells, not in conventional CD8⁺ or NK cells.
Targeting the PUFA–lipid peroxide axis represents a targetable metabolic checkpoint to enhance immunotherapy in HCC.
Targeting the PUFA–lipid peroxide axis represents a targetable metabolic checkpoint to enhance immunotherapy in HCC.
MASLD generates a lipid-driven immunosuppressive microenvironment by inducing metabolic exhaustion-mediated dysfunction and ferroptosis in MAIT cells—an abundant intrahepatic T cell subset with anti-tumour properties.
MASLD generates a lipid-driven immunosuppressive microenvironment by inducing metabolic exhaustion-mediated dysfunction and ferroptosis in MAIT cells—an abundant intrahepatic T cell subset with anti-tumour properties.
• Interfering with lipid peroxide formation reverses MAIT dysfunction and restores anti-cancer activity.
• A PUFA-MAIT cell gene signature correlates with poor overall survival of patients with HCC.
• Interfering with lipid peroxide formation reverses MAIT dysfunction and restores anti-cancer activity.
• A PUFA-MAIT cell gene signature correlates with poor overall survival of patients with HCC.
• PUFAs induce intracellular lipid peroxidation, driving metabolic exhaustion – mitochondrial and glycolytic dysfunction – and triggering ferroptosis.
• PUFAs induce intracellular lipid peroxidation, driving metabolic exhaustion – mitochondrial and glycolytic dysfunction – and triggering ferroptosis.
• In MASLD, MAIT cells exhibit profound functional exhaustion, including impaired cytokine production and anti-tumour activity.
• Mechanistically, PUFAs accumulate selectively in MAIT cells, not in conventional CD8⁺ or NK cells.
• In MASLD, MAIT cells exhibit profound functional exhaustion, including impaired cytokine production and anti-tumour activity.
• Mechanistically, PUFAs accumulate selectively in MAIT cells, not in conventional CD8⁺ or NK cells.