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View article: Decades-long elevation of interferon-α drives a Sjögren disease endotype: an interdisciplinary study
Decades-long elevation of interferon-α drives a Sjögren disease endotype: an interdisciplinary study Open
SUMMARY BACKGROUND Mechanistic heterogeneity is a major obstacle to the development of effective treatment for Sjögren disease (SjD) and there is a pressing need to stratify SjD according to precision medicine principles. Aberrant activati…
View article: Figure S9 from Systemic Inactivation of TREX1 Induces Selective Inflammation of the Tumor Microenvironment and Invigorated T-cell–Mediated Tumor Control
Figure S9 from Systemic Inactivation of TREX1 Induces Selective Inflammation of the Tumor Microenvironment and Invigorated T-cell–Mediated Tumor Control Open
Figure S9 shows that TREX1-/- B16.F10 cells have normal growth in vitro, do not spontaneously produce IFN, but feature enhanced responsiveness to transfected DNA.
View article: Figure S8 from Systemic Inactivation of TREX1 Induces Selective Inflammation of the Tumor Microenvironment and Invigorated T-cell–Mediated Tumor Control
Figure S8 from Systemic Inactivation of TREX1 Induces Selective Inflammation of the Tumor Microenvironment and Invigorated T-cell–Mediated Tumor Control Open
Figure S8 shows single cell data on the invigorated intra-tumoral CD8 T cell response upon loss of TREX1 in the host.
View article: Figure S2 from Systemic Inactivation of TREX1 Induces Selective Inflammation of the Tumor Microenvironment and Invigorated T-cell–Mediated Tumor Control
Figure S2 from Systemic Inactivation of TREX1 Induces Selective Inflammation of the Tumor Microenvironment and Invigorated T-cell–Mediated Tumor Control Open
Figure S2 shows gating of immune cell populations in tumor tissue as well as quantification of immune cells in tumor, tumor-draining lymph node and spleen.
View article: Figure S6 from Systemic Inactivation of TREX1 Induces Selective Inflammation of the Tumor Microenvironment and Invigorated T-cell–Mediated Tumor Control
Figure S6 from Systemic Inactivation of TREX1 Induces Selective Inflammation of the Tumor Microenvironment and Invigorated T-cell–Mediated Tumor Control Open
Figure S6 shows the inflammatory switch of the intra-tumoral myeloid compartment in TREX1 iKO hosts.
View article: Data from Systemic Inactivation of TREX1 Induces Selective Inflammation of the Tumor Microenvironment and Invigorated T-cell–Mediated Tumor Control
Data from Systemic Inactivation of TREX1 Induces Selective Inflammation of the Tumor Microenvironment and Invigorated T-cell–Mediated Tumor Control Open
Therapeutic innate immune-stimulation within the tumor microenvironment can potentiate endogenous antitumor T-cell immunity. Strategies for controlled activation of cGAS/STING signaling are currently under intense investigation. DNase 3′-r…
View article: Figure S1 from Systemic Inactivation of TREX1 Induces Selective Inflammation of the Tumor Microenvironment and Invigorated T-cell–Mediated Tumor Control
Figure S1 from Systemic Inactivation of TREX1 Induces Selective Inflammation of the Tumor Microenvironment and Invigorated T-cell–Mediated Tumor Control Open
Figure S1 shows efficiency of induced TREX1 deletion and how induced loss of TREX1 impacts growth of MB49 tumors.
View article: Figure S5 from Systemic Inactivation of TREX1 Induces Selective Inflammation of the Tumor Microenvironment and Invigorated T-cell–Mediated Tumor Control
Figure S5 from Systemic Inactivation of TREX1 Induces Selective Inflammation of the Tumor Microenvironment and Invigorated T-cell–Mediated Tumor Control Open
Figure S5 shows efficiency of IFNAR blockade and of CD8 T cell and NK cell depletion in different tissues of the host.
View article: Figure S4 from Systemic Inactivation of TREX1 Induces Selective Inflammation of the Tumor Microenvironment and Invigorated T-cell–Mediated Tumor Control
Figure S4 from Systemic Inactivation of TREX1 Induces Selective Inflammation of the Tumor Microenvironment and Invigorated T-cell–Mediated Tumor Control Open
Figure S4 shows absence of inflammation of non-tumor tissues upon Trex1 iKO.
View article: Figure S3 from Systemic Inactivation of TREX1 Induces Selective Inflammation of the Tumor Microenvironment and Invigorated T-cell–Mediated Tumor Control
Figure S3 from Systemic Inactivation of TREX1 Induces Selective Inflammation of the Tumor Microenvironment and Invigorated T-cell–Mediated Tumor Control Open
Figure S3 shows cluster-defining genes of tumor-infiltrating immune cells (scRNAseq) as well as impact of TREX1 iKO on immune populations size and on ISG expression.
View article: Figure S7 from Systemic Inactivation of TREX1 Induces Selective Inflammation of the Tumor Microenvironment and Invigorated T-cell–Mediated Tumor Control
Figure S7 from Systemic Inactivation of TREX1 Induces Selective Inflammation of the Tumor Microenvironment and Invigorated T-cell–Mediated Tumor Control Open
Figure S7 shows data on the intra-tumoral immune cell compartment in mice constitutively lacking TREX1 in conventional dendritic cells.
View article: CSF1R+ myeloid-monocytic cells drive CAR-T cell resistance in aggressive B cell lymphoma
CSF1R+ myeloid-monocytic cells drive CAR-T cell resistance in aggressive B cell lymphoma Open
Despite the improvement, approximately 60% of patients with relapsed or refractory (r/r) aggressive B cell lymphoma (B-NHL) do not achieve durable benefit from CAR-T cell therapy. To elucidate factors associated with CAR-T therapy resistan…
View article: Mast cells modulate macrophage biology through release of prestored CSF1
Mast cells modulate macrophage biology through release of prestored CSF1 Open
CSF1 is an evolutionarily conserved, constitutive MC granule component. MC degranulation induces macrophage differentiation and a unique polarization state, the former being completely dependent on CSF1, whereas the latter is only modulate…
View article: TGF-β drives differentiation of intraepithelial mast cells in inflamed airway mucosa
TGF-β drives differentiation of intraepithelial mast cells in inflamed airway mucosa Open
Similarly to acute intestinal helminth infection, several conditions of chronic eosinophilic type 2 inflammation of mucosal surfaces, including asthma and eosinophilic esophagitis, feature robust expansions of intraepithelial mast cells (M…
View article: Targeting Lymphoma Associated Myeloid-Monocytic Cells through CSF1R Blockade Enhances CAR-T Cell Response in Aggressive B Cell Lymphoma
Targeting Lymphoma Associated Myeloid-Monocytic Cells through CSF1R Blockade Enhances CAR-T Cell Response in Aggressive B Cell Lymphoma Open
Introduction: Chimeric antigen receptor (CAR) T cell therapy has substantially improved the outcome of patients suffering from relapsed and/or refractory (r/r) aggressive B cell lymphoma. However, around 60% of patients do not show long-te…
View article: Supplementary Data from Activation of the cGAS/STING axis in genome-damaged hematopoietic cells does not impact blood cell formation or leukemogenesis
Supplementary Data from Activation of the cGAS/STING axis in genome-damaged hematopoietic cells does not impact blood cell formation or leukemogenesis Open
Supplementary Figures S1-8 and corresponding figure legends
View article: Table S1 from Activation of the cGAS/STING axis in genome-damaged hematopoietic cells does not impact blood cell formation or leukemogenesis
Table S1 from Activation of the cGAS/STING axis in genome-damaged hematopoietic cells does not impact blood cell formation or leukemogenesis Open
List of antibodies used in the study
View article: Table S2 from Activation of the cGAS/STING axis in genome-damaged hematopoietic cells does not impact blood cell formation or leukemogenesis
Table S2 from Activation of the cGAS/STING axis in genome-damaged hematopoietic cells does not impact blood cell formation or leukemogenesis Open
Oligo nucleotide sequences
View article: Supplementary Tables S3-5 from Activation of the cGAS/STING axis in genome-damaged hematopoietic cells does not impact blood cell formation or leukemogenesis
Supplementary Tables S3-5 from Activation of the cGAS/STING axis in genome-damaged hematopoietic cells does not impact blood cell formation or leukemogenesis Open
Transcriptome analysis
View article: Table S1 from Activation of the cGAS/STING axis in genome-damaged hematopoietic cells does not impact blood cell formation or leukemogenesis
Table S1 from Activation of the cGAS/STING axis in genome-damaged hematopoietic cells does not impact blood cell formation or leukemogenesis Open
List of antibodies used in the study
View article: Data from Activation of the cGAS/STING axis in genome-damaged hematopoietic cells does not impact blood cell formation or leukemogenesis
Data from Activation of the cGAS/STING axis in genome-damaged hematopoietic cells does not impact blood cell formation or leukemogenesis Open
Genome damage is a main driver of malignant transformation, but it also induces aberrant inflammation via the cGAS/STING DNA sensing pathway. Activation of cGAS/STING can trigger cell death and senescence, thereby potentially eliminating g…
View article: Supplementary Tables S3-5 from Activation of the cGAS/STING axis in genome-damaged hematopoietic cells does not impact blood cell formation or leukemogenesis
Supplementary Tables S3-5 from Activation of the cGAS/STING axis in genome-damaged hematopoietic cells does not impact blood cell formation or leukemogenesis Open
Transcriptome analysis
View article: Supplementary Data from Activation of the cGAS/STING axis in genome-damaged hematopoietic cells does not impact blood cell formation or leukemogenesis
Supplementary Data from Activation of the cGAS/STING axis in genome-damaged hematopoietic cells does not impact blood cell formation or leukemogenesis Open
Supplementary Figures S1-8 and corresponding figure legends
View article: Table S2 from Activation of the cGAS/STING axis in genome-damaged hematopoietic cells does not impact blood cell formation or leukemogenesis
Table S2 from Activation of the cGAS/STING axis in genome-damaged hematopoietic cells does not impact blood cell formation or leukemogenesis Open
Oligo nucleotide sequences
View article: Selective inflammation of the tumor microenvironment and invigorated T cell-mediated tumor control upon induced systemic inactivation of TREX1
Selective inflammation of the tumor microenvironment and invigorated T cell-mediated tumor control upon induced systemic inactivation of TREX1 Open
Therapeutic innate immune stimulation within the tumor microenvironment can potentiate endogenous antitumor T cell immunity. DNase 3’-repair exonuclease 1 (TREX1) is essential for cellular DNA disposal which prevents autoimmunity ensuing f…
View article: Aberrant RNA sensing in regulatory T cells causes systemic autoimmunity
Aberrant RNA sensing in regulatory T cells causes systemic autoimmunity Open
Chronic and aberrant nucleic acid sensing causes type I IFN–driven autoimmune diseases, designated type I interferonopathies. We found a significant reduction of regulatory T cells (T regs ) in patients with type I interferonopathies cause…
View article: High population frequencies of MICA copy number variations originate from independent recombination events
High population frequencies of MICA copy number variations originate from independent recombination events Open
MICA is a stress-induced ligand of the NKG2D receptor that stimulates NK and T cell responses and was identified as a key determinant of anti-tumor immunity. The MICA gene is located inside the MHC complex and is in strong linkage disequil…