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View article: Reprogramming autoimmunity: inducing antigen-specific tolerance via apoptotic mimicry in an experimental model of multiple sclerosis
Reprogramming autoimmunity: inducing antigen-specific tolerance via apoptotic mimicry in an experimental model of multiple sclerosis Open
Our findings indicate that antigen-specific therapy with PS liposomes mimicking apoptotic bodies downregulates the MOG-specific inflammatory immune response and expands Breg and Treg cells, offering a safe, versatile, and easily applicable…
View article: Cladribine Preserves Normal Central Nervous System Cellular Activity and Promotes Neuroprotection to Oxidative Stress Damage
Cladribine Preserves Normal Central Nervous System Cellular Activity and Promotes Neuroprotection to Oxidative Stress Damage Open
Multiple sclerosis (MS) is a chronic neuroinflammatory and demyelinating disease that causes disability in patients. Cladribine is an oral treatment that is used in relapsing–remitting and active secondary progressive MS. T and B lymphocyt…
View article: Targeting T cell modulation with novel bile acid derivatives in autoimmunity 2982
Targeting T cell modulation with novel bile acid derivatives in autoimmunity 2982 Open
Description Recent research identified derivatives of lithocholic acid (LCA) as immunomodulators of T cell differentiation. Specifically, 3-oxoLCA and isoLCA inhibit Th17 cells, while isoalloLCA promotes Treg cells in the absence of antige…
View article: Multiple sclerosis: molecular pathogenesis and therapeutic intervention
Multiple sclerosis: molecular pathogenesis and therapeutic intervention Open
Multiple sclerosis is a chronic immune-mediated disorder of the central nervous system characterized by demyelination, axonal loss, and neuroinflammation, culminating in progressive neurological disability. Despite significant advances in …
View article: Figure S3 from Harnessing STING Signaling and Natural Killer Cells Overcomes PARP Inhibitor Resistance in Homologous Recombination–Deficient Breast Cancer
Figure S3 from Harnessing STING Signaling and Natural Killer Cells Overcomes PARP Inhibitor Resistance in Homologous Recombination–Deficient Breast Cancer Open
Same HRR functionality, PARP enzymatic inhibition and DNA damage in different mouse strains
View article: Figure S4 from Harnessing STING Signaling and Natural Killer Cells Overcomes PARP Inhibitor Resistance in Homologous Recombination–Deficient Breast Cancer
Figure S4 from Harnessing STING Signaling and Natural Killer Cells Overcomes PARP Inhibitor Resistance in Homologous Recombination–Deficient Breast Cancer Open
Analysis of the mechanism of PARPi resistance in MDA594ORs
View article: Figure S5 from Harnessing STING Signaling and Natural Killer Cells Overcomes PARP Inhibitor Resistance in Homologous Recombination–Deficient Breast Cancer
Figure S5 from Harnessing STING Signaling and Natural Killer Cells Overcomes PARP Inhibitor Resistance in Homologous Recombination–Deficient Breast Cancer Open
MDA single cells annotation in cell types
View article: Data from Harnessing STING Signaling and Natural Killer Cells Overcomes PARP Inhibitor Resistance in Homologous Recombination–Deficient Breast Cancer
Data from Harnessing STING Signaling and Natural Killer Cells Overcomes PARP Inhibitor Resistance in Homologous Recombination–Deficient Breast Cancer Open
Homologous recombination deficiency (HRD) contributes to genomic instability and leads to sensitivity to PARP inhibitors (PARPi). HRD also activates the cyclic GMP–AMP synthase (cGAS)–stimulator of interferon genes (STING)–interferon pathw…
View article: Table S4 from Harnessing STING Signaling and Natural Killer Cells Overcomes PARP Inhibitor Resistance in Homologous Recombination–Deficient Breast Cancer
Table S4 from Harnessing STING Signaling and Natural Killer Cells Overcomes PARP Inhibitor Resistance in Homologous Recombination–Deficient Breast Cancer Open
Patient cohort
View article: Table S1 from Harnessing STING Signaling and Natural Killer Cells Overcomes PARP Inhibitor Resistance in Homologous Recombination–Deficient Breast Cancer
Table S1 from Harnessing STING Signaling and Natural Killer Cells Overcomes PARP Inhibitor Resistance in Homologous Recombination–Deficient Breast Cancer Open
PDX cohort
View article: Figure S12 from Harnessing STING Signaling and Natural Killer Cells Overcomes PARP Inhibitor Resistance in Homologous Recombination–Deficient Breast Cancer
Figure S12 from Harnessing STING Signaling and Natural Killer Cells Overcomes PARP Inhibitor Resistance in Homologous Recombination–Deficient Breast Cancer Open
PARPi affects the peripheral immune composition in patients
View article: Figure S7 from Harnessing STING Signaling and Natural Killer Cells Overcomes PARP Inhibitor Resistance in Homologous Recombination–Deficient Breast Cancer
Figure S7 from Harnessing STING Signaling and Natural Killer Cells Overcomes PARP Inhibitor Resistance in Homologous Recombination–Deficient Breast Cancer Open
Coupled single cell RNA and TCR sequencing reveals hyperexpanded TCR clonotypes expressing tumor related signatures
View article: Figure S6 from Harnessing STING Signaling and Natural Killer Cells Overcomes PARP Inhibitor Resistance in Homologous Recombination–Deficient Breast Cancer
Figure S6 from Harnessing STING Signaling and Natural Killer Cells Overcomes PARP Inhibitor Resistance in Homologous Recombination–Deficient Breast Cancer Open
Interferon responses up-regulation in MDA tumor microenvironment
View article: Figure S11 from Harnessing STING Signaling and Natural Killer Cells Overcomes PARP Inhibitor Resistance in Homologous Recombination–Deficient Breast Cancer
Figure S11 from Harnessing STING Signaling and Natural Killer Cells Overcomes PARP Inhibitor Resistance in Homologous Recombination–Deficient Breast Cancer Open
Image analysis of tissue cyclic immunofluorescence in HRR-altered patients
View article: Table S3 from Harnessing STING Signaling and Natural Killer Cells Overcomes PARP Inhibitor Resistance in Homologous Recombination–Deficient Breast Cancer
Table S3 from Harnessing STING Signaling and Natural Killer Cells Overcomes PARP Inhibitor Resistance in Homologous Recombination–Deficient Breast Cancer Open
Bulk RNA sequencing of PDX230OR8 tumors
View article: Figure S1 from Harnessing STING Signaling and Natural Killer Cells Overcomes PARP Inhibitor Resistance in Homologous Recombination–Deficient Breast Cancer
Figure S1 from Harnessing STING Signaling and Natural Killer Cells Overcomes PARP Inhibitor Resistance in Homologous Recombination–Deficient Breast Cancer Open
STING-related biomarkers in BC PDXs
View article: Figure S10 from Harnessing STING Signaling and Natural Killer Cells Overcomes PARP Inhibitor Resistance in Homologous Recombination–Deficient Breast Cancer
Figure S10 from Harnessing STING Signaling and Natural Killer Cells Overcomes PARP Inhibitor Resistance in Homologous Recombination–Deficient Breast Cancer Open
Natural Killer (NK) cells depletion in vivo
View article: Figure S9 from Harnessing STING Signaling and Natural Killer Cells Overcomes PARP Inhibitor Resistance in Homologous Recombination–Deficient Breast Cancer
Figure S9 from Harnessing STING Signaling and Natural Killer Cells Overcomes PARP Inhibitor Resistance in Homologous Recombination–Deficient Breast Cancer Open
Generation of PDX230OR8 and analysis of the mechanism of PARPi resistance
View article: Figure S13 from Harnessing STING Signaling and Natural Killer Cells Overcomes PARP Inhibitor Resistance in Homologous Recombination–Deficient Breast Cancer
Figure S13 from Harnessing STING Signaling and Natural Killer Cells Overcomes PARP Inhibitor Resistance in Homologous Recombination–Deficient Breast Cancer Open
Coupled scRNA-seq and scTCR-seq in peripheral blood identified hyperexpanded TCR clonotypes in the CD8 cytotoxic and NK-like T cells subsets
View article: Table S2 from Harnessing STING Signaling and Natural Killer Cells Overcomes PARP Inhibitor Resistance in Homologous Recombination–Deficient Breast Cancer
Table S2 from Harnessing STING Signaling and Natural Killer Cells Overcomes PARP Inhibitor Resistance in Homologous Recombination–Deficient Breast Cancer Open
Bulk RNA sequencing of Mouse Derived Allograft (MDA) tumors.
View article: Figure S2 from Harnessing STING Signaling and Natural Killer Cells Overcomes PARP Inhibitor Resistance in Homologous Recombination–Deficient Breast Cancer
Figure S2 from Harnessing STING Signaling and Natural Killer Cells Overcomes PARP Inhibitor Resistance in Homologous Recombination–Deficient Breast Cancer Open
Up-regulation of Interferon Stimulated Genes (ISGs) in PARPi-sensitive PDX models
View article: Figure S8 from Harnessing STING Signaling and Natural Killer Cells Overcomes PARP Inhibitor Resistance in Homologous Recombination–Deficient Breast Cancer
Figure S8 from Harnessing STING Signaling and Natural Killer Cells Overcomes PARP Inhibitor Resistance in Homologous Recombination–Deficient Breast Cancer Open
Combination of PARPi and STINGa in vivo
View article: Harnessing STING Signaling and Natural Killer Cells Overcomes PARP Inhibitor Resistance in Homologous Recombination–Deficient Breast Cancer
Harnessing STING Signaling and Natural Killer Cells Overcomes PARP Inhibitor Resistance in Homologous Recombination–Deficient Breast Cancer Open
Homologous recombination deficiency (HRD) contributes to genomic instability and leads to sensitivity to PARP inhibitors (PARPi). HRD also activates the cyclic GMP–AMP synthase (cGAS)–stimulator of interferon genes (STING)–interferon pathw…
View article: Disease Aggravation With Age in an Experimental Model of Multiple Sclerosis: Role of Immunosenescence
Disease Aggravation With Age in an Experimental Model of Multiple Sclerosis: Role of Immunosenescence Open
The onset of multiple sclerosis (MS) in older individuals correlates with a higher risk of developing primary progressive MS, faster progression to secondary progressive MS, and increased disability accumulation. This phenomenon can be rel…
View article: IL-6 Inhibition as a Therapeutic Target in Aged Experimental Autoimmune Encephalomyelitis
IL-6 Inhibition as a Therapeutic Target in Aged Experimental Autoimmune Encephalomyelitis Open
Multiple sclerosis (MS) onset at an advanced age is associated with a higher risk of developing progressive forms and a greater accumulation of disability for which there are currently no effective disease-modifying treatments. Immunosenes…
View article: Molecular signature associated with cladribine treatment in patients with multiple sclerosis
Molecular signature associated with cladribine treatment in patients with multiple sclerosis Open
Introduction Little is known about the molecular profiling associated with the effect of cladribine in patients with multiple sclerosis (MS). Here, we aimed first to characterize the transcriptomic and proteomic profiles induced by cladrib…
View article: Therapeutic Effect of IL-21 Blockage by Gene Therapy in Experimental Autoimmune Encephalomyelitis
Therapeutic Effect of IL-21 Blockage by Gene Therapy in Experimental Autoimmune Encephalomyelitis Open
The pathogenic role of the interleukin 21 (IL-21) in different autoimmune diseases, such as multiple sclerosis (MS), has been extensively studied. However, its pleiotropic nature makes it a cytokine that may exhibit different activity depe…
View article: Immunomodulatory Effects Associated with Cladribine Treatment
Immunomodulatory Effects Associated with Cladribine Treatment Open
Cladribine is a synthetic deoxyadenosine analogue with demonstrated efficacy in patients with relapsing-remitting multiple sclerosis (MS). The main mechanism of action described for cladribine is the induction of a cytotoxic effect on lymp…
View article: Immunosenescence in multiple sclerosis: the identification of new therapeutic targets
Immunosenescence in multiple sclerosis: the identification of new therapeutic targets Open
The number of elderly multiple sclerosis (MS) patients is growing, mainly due to the increase in the life expectancy of the general population and the availability of effective disease-modifying treatments. However, current treatments redu…