Michael Sanford

ORCID: 0000-0002-9411-2606
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Research Areas
  • Immune cells in cancer
  • Chemokine receptors and signaling
  • Systemic Lupus Erythematosus Research
  • Immunotherapy and Immune Responses
  • Immune Cell Function and Interaction
  • T-cell and B-cell Immunology
  • Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Reproductive System and Pregnancy
  • Liver Disease Diagnosis and Treatment
  • Cancer Immunotherapy and Biomarkers
  • Liver Diseases and Immunity
  • RNA Interference and Gene Delivery
  • interferon and immune responses
  • Immune Response and Inflammation
  • Cytokine Signaling Pathways and Interactions
  • Advanced biosensing and bioanalysis techniques
  • IL-33, ST2, and ILC Pathways
  • Antimicrobial Peptides and Activities
  • Monoclonal and Polyclonal Antibodies Research
  • Bacterial Infections and Vaccines
  • Tissue Engineering and Regenerative Medicine
  • Mitochondrial Function and Pathology
  • Muscle Physiology and Disorders
  • Genetic Neurodegenerative Diseases
  • Single-cell and spatial transcriptomics

Center for Cancer Research
2005-2024

National Cancer Institute
2005-2024

Frederick National Laboratory for Cancer Research
2001-2024

National Institutes of Health
2024

Leidos (United States)
2017

Science Applications International Corporation (United States)
2005

Abstract We previously demonstrated that agents known to signal infection or inflammation can rapidly and directly drive differentiation of human CD14+ monocytes into CD83+ dendritic cells (DCs) when introduced under serum-free conditions. In this study, we evaluated the effects TGF-β vitamin D3 (VitD3) on proportion function adopt DC characteristics. significantly decreased adopted stable characteristics in response LPS, but had little no effect calcium ionophore-induced differentiation....

10.4049/jimmunol.174.4.2061 article EN The Journal of Immunology 2005-02-15

Abstract We present a remodeling method for high-affinity unnatural-base DNA aptamers to augment their thermal stability and nuclease resistance, use as drug candidates targeting specific proteins. Introducing unique mini-hairpin provides robust generated by SELEX using genetic alphabet expansion, without reducing high affinity. By this method, >80% of the remodeled aptamer interferon-γ ( K D 33 pM) survived in human serum at 37 °C after 3 days under our experimental conditions...

10.1038/srep18478 article EN cc-by Scientific Reports 2015-12-22

We have reported on a murine model of autoimmune cholangitis, generated by altering the AU-rich element (ARE) deletion interferon gamma (IFN-γ) 3' untranslated region (coined ARE-Del-/- ), that has striking similarities to human primary biliary cholangitis (PBC) with female predominance. Previously, we suggested sex bias was secondary intense and sustained type I II IFN signaling. Based this thesis, define mechanisms lead portal inflammation, specifically addressed hypothesis IFNs are driver...

10.1002/hep.29524 article EN Hepatology 2017-09-18

Abstract Mammalian antimicrobial peptides, including β-defensins, represent an ancient arm of innate immunity designed to directly neutralize invading microbes. Previously, we demonstrated that murine β-defensin 2 (mDF2β) also acted as endogenous ligand for TLR-4-activating maturation dendritic cells (DCs). Herein, report this TLR-4 –dependent activation leads induction atypical cell death is unexpectedly exaggerated by the inhibition caspases. Experiments using APCs with nonfunctional TNF-α...

10.1189/jlb.1007700 article EN Journal of Leukocyte Biology 2008-01-11

Introduction Interferon-gamma (IFN-γ) is pivotal in orchestrating immune responses during healthy pregnancy. However, its dysregulation, often due to autoimmunity, infections, or chronic inflammatory conditions, implicated adverse reproductive outcomes such as pregnancy failure infertility. Additionally, the underlying immunological mechanisms remain elusive. Methods Here, we explore impact of systemic IFN-γ elevation on cytotoxic T cell female reproduction utilizing a lupus-prone mouse...

10.3389/fimmu.2024.1368572 article EN cc-by Frontiers in Immunology 2024-04-18

Abstract The relationship between cancer and autoimmunity is complex. However, the incidence of solid tumors such as melanoma has increased significantly among patients with previous or newly diagnosed systemic autoimmune disease (AID). At same time, immune checkpoint blockade (ICB) therapy induces de novo autoinflammation exacerbates underlying AID, even without evident antitumor responses. Recently, lupus erythematosus (SLE) activity was found to drive myeloid-derived suppressor cell...

10.1158/0008-5472.can-21-1148 article EN Cancer Research 2021-10-12

Abstract The effect of cytokines on non‐traditional immunological targets under conditions chronic inflammation is an ongoing subject study. Fatigue a symptom often associated with autoimmune diseases. Chronic inflammatory response and activated cell‐mediated immunity are cardiovascular myopathies which can be driven by muscle weakness fatigue. Thus, we hypothesize that immune dysfunction‐driven changes in myocyte mitochondria may play critical role fatigue‐related pathogenesis. We show...

10.1002/path.6081 article EN The Journal of Pathology 2023-04-27

Here, we present a validated workflow to isolate sufficient viable single ovary cells from mouse without the need pool several mice. We provide steps essential for estrous staging, harvesting and dissociation, cell staining, data collection, analysis. Our approach allows use of these single-cell suspensions flow sorting, cytometry analysis, or functional in vitro assays. Importantly, our protocol is designed maximize isolation immune cells, including T subsets.

10.1016/j.xpro.2023.102710 article EN cc-by-nc-nd STAR Protocols 2023-11-14

Abstract We generated a mouse model with 162 nt AU-rich element (ARE) region deletion in the 3’ untranslated (3’UTR) of interferon (IFN)-gamma gene that results chronic circulating serum IFN-gamma levels. Mice homozygous for ARE present both serologic and cellular abnormalities typical patients systemic lupus erythematosus (SLE). Marginal zone B (MZB) cells marginal macrophages (MZMs) are absent ARE-deleted (ARE-Del)-/- mice. ARE-Del+/- mice retain MZB MZMs develop no or mild autoimmunity....

10.4049/jimmunol.192.supp.179.1 article EN The Journal of Immunology 2014-05-01

<div>Abstract<p>The relationship between cancer and autoimmunity is complex. However, the incidence of solid tumors such as melanoma has increased significantly among patients with previous or newly diagnosed systemic autoimmune disease (AID). At same time, immune checkpoint blockade (ICB) therapy induces <i>de novo</i> autoinflammation exacerbates underlying AID, even without evident antitumor responses. Recently, lupus erythematosus (SLE) activity was found to drive...

10.1158/0008-5472.c.6513930.v1 preprint EN 2023-03-31

Abstract The overlapping signatures of type 1 interferons (IFN) and IFN-gamma (IFNg) has proven challenging in human autoimmunity cancer immunotherapy, particularly for resistance to anti-programmed death (anti-PD1) monotherapy. By contrast, agonist abs targeting CD40 (anti-CD40) antibodies (abs) clinically elicit anti-tumor immunity with limited autoimmune complications. Here, we explore the relationships between anti-PD1 or responses melanoma tumors from IFN alpha receptor...

10.1158/1538-7445.am2023-5138 article EN Cancer Research 2023-04-04

<div>Abstract<p>The relationship between cancer and autoimmunity is complex. However, the incidence of solid tumors such as melanoma has increased significantly among patients with previous or newly diagnosed systemic autoimmune disease (AID). At same time, immune checkpoint blockade (ICB) therapy induces <i>de novo</i> autoinflammation exacerbates underlying AID, even without evident antitumor responses. Recently, lupus erythematosus (SLE) activity was found to drive...

10.1158/0008-5472.c.6513930 preprint EN 2023-03-31

You have accessJournal of UrologyDiscussed Poster, Sunday, May 9, 2004, 1:00 - 5:00 pm1 Apr 2004577: Investigation Acellular Dermal Matrix for the Correction Reflux Richard N. Schlussel, and Michael Sanford SchlusselRichard Schlussel More articles by this author , SanfordMichael View All Author Informationhttps://doi.org/10.1016/S0022-5347(18)37839-XAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail "577: Reflux." The Journal...

10.1016/s0022-5347(18)37839-x article EN The Journal of Urology 2004-04-01
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