A5055327401- Cancer Immunotherapy and Biomarkers
- interferon and immune responses
- Immune cells in cancer
- CAR-T cell therapy research
- Viral Infections and Vectors
- Immunotherapy and Immune Responses
- Phagocytosis and Immune Regulation
- Immune Cell Function and Interaction
- Mosquito-borne diseases and control
- Tryptophan and brain disorders
- Single-cell and spatial transcriptomics
- Mathematical Biology Tumor Growth
- Cancer Genomics and Diagnostics
- Epigenetics and DNA Methylation
- Renal cell carcinoma treatment
- Monoclonal and Polyclonal Antibodies Research
- Inflammasome and immune disorders
- Atherosclerosis and Cardiovascular Diseases
- Prenatal Screening and Diagnostics
- Lower Extremity Biomechanics and Pathologies
- Muscle activation and electromyography studies
- Cancer Research and Treatments
- Ferroptosis and cancer prognosis
- Pancreatic and Hepatic Oncology Research
- CRISPR and Genetic Engineering
Jackson Laboratory
2011-2021
Inserm
2009
Hospital Universitario de La Princesa
2009
Western Washington University
2006
Checkpoint inhibitors like anti-PD1/PD-L1 have demonstrated significant therapeutic efficacy in a subset of patients partly through reinvigoration CD8 T cells. However, their impact on myeloid cells remains largely unknown. Here, we report that anti-PD-L1 treatment favorably impacts the phenotype and function tumor macrophages by polarizing macrophage compartment toward more proinflammatory phenotype. This was characterized decrease Arginase-I (ARG1) expression an increase iNOS, MHCII, CD40...
Abstract The DNA exonuclease three-prime repair 1 (TREX1) is critical for preventing autoimmunity in mice and humans by degrading endogenous cytosolic DNA, which otherwise triggers activation of the innate cGAS/STING pathway leading to production type I IFNs. As tumor cells are prone aberrant accumulation, we hypothesized that they critically dependent on TREX1 activity limit their immunogenicity. Here, show cells, restricts spontaneous pathway, subsequent induction a IFN response. result,...
Exhausted T cells have been described in cancer patients and murine tumor models largely based on their expression of various inhibitory receptors. Understanding the functional attributes these is limited. Here, we report that among CD8+ commonly used syngeneic models, coexpression receptors PD-1, LAG3, TIM3 defined a group highly activated effector cells. Coexpression further enriched for antigen-specific with increased T-cell receptor clonality. Anti-PD-L1 treatment number activation...
Background Cancer immunotherapy has evolved from interferon-alpha (IFNα) and interleukin-2 in the 1980s to CTLA-4 PD-1/PD-L1 checkpoint inhibitors (CPIs), latter highlighting importance of enhancing T-cell functions. While search for novel immunomodulatory pathways continues, combination therapies augmenting multiple can also increase efficacy. The association autoimmune-related adverse events with clinical efficacy following CPI treatment been inferred suggests that breaking tolerance...
<div>Abstract<p>The DNA exonuclease three-prime repair 1 (TREX1) is critical for preventing autoimmunity in mice and humans by degrading endogenous cytosolic DNA, which otherwise triggers activation of the innate cGAS/STING pathway leading to production type I IFNs. As tumor cells are prone aberrant accumulation, we hypothesized that they critically dependent on TREX1 activity limit their immunogenicity. Here, show cells, restricts spontaneous pathway, subsequent induction a IFN...
Renal medullary carcinoma (RMC) is a rare but aggressive tumor often complicated by early lung metastasis with few treatment options and very poor outcomes. There are currently no verified RMC patient-derived xenograft (PDX) mouse models established from metastatic pleural effusion (PE) available to study evaluate new therapeutic options. tissue malignant PE cells an patient were successfully engrafted into 20 NOD.Cg-Prkdcscid Il2rgtm1Wjl/SzJ (NSG) mice. We evaluated the histopathological...
Abstract The DNA exonuclease TREX1 (Three-prime repair 1) is critical for preventing autoimmunity in mice and humans by degrading endogenous cytosolic DNA, which otherwise triggers activation of the innate cGAS/STING pathway leading to production type I IFNs. Since tumor cells are prone aberrant accumulation, we hypothesized that they critically dependent on activity limit their immunogenicity. Here show, indeed restricts spontaneous subsequent induction a IFN response. As result, deficiency...
<p>Supplementary Figure 1. TREX1 limits an ISG response in CT26 and STING-expressing MC38 cells.</p>
<p>Supplementary Figure 5. TREX1 loss remodels an immunosuppressive myeloid tumor microenvironment</p>
<p>Supplementary Figure 4. Single-cell RNA sequencing workflow and ISG expression across immune cells in the tumor microenvironment</p>
<p>Supplementary Figure 2. Tumor-intrinsic TREX1 loss impairs CT26 tumor growth in immunocompetent mice a cGAS dependent manner.</p>
<p>Supplementary Figure 1. TREX1 limits an ISG response in CT26 and STING-expressing MC38 cells.</p>
<p>Supplementary Figure 6. TREX1 loss increases CD8 T cell and NK activation, limits exhaustion enhances the potency of immune checkpoint blockade therapy</p>
<p>Supplementary Figure 3. Assessment of TREX1’s catalytic activity and cGAS dependency.</p>
<p>Supplementary Figure 5. TREX1 loss remodels an immunosuppressive myeloid tumor microenvironment</p>
<p>Supplementary Figure 6. TREX1 loss increases CD8 T cell and NK activation, limits exhaustion enhances the potency of immune checkpoint blockade therapy</p>
<p>Supplementary Figure 2. Tumor-intrinsic TREX1 loss impairs CT26 tumor growth in immunocompetent mice a cGAS dependent manner.</p>
<p>Supplementary Figure 4. Single-cell RNA sequencing workflow and ISG expression across immune cells in the tumor microenvironment</p>
<p>Supplementary Figure 3. Assessment of TREX1’s catalytic activity and cGAS dependency.</p>
<div>Abstract<p>The DNA exonuclease three-prime repair 1 (TREX1) is critical for preventing autoimmunity in mice and humans by degrading endogenous cytosolic DNA, which otherwise triggers activation of the innate cGAS/STING pathway leading to production type I IFNs. As tumor cells are prone aberrant accumulation, we hypothesized that they critically dependent on TREX1 activity limit their immunogenicity. Here, show cells, restricts spontaneous pathway, subsequent induction a IFN...