David Jesse Sanchez

ORCID: 0000-0002-6032-4600
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About
Contact & Profiles
Research Areas
  • interferon and immune responses
  • Cytomegalovirus and herpesvirus research
  • Immune Cell Function and Interaction
  • HIV Research and Treatment
  • Viral-associated cancers and disorders
  • Herpesvirus Infections and Treatments
  • Viral Infections and Immunology Research
  • Animal Disease Management and Epidemiology
  • Hepatitis C virus research
  • Immunotherapy and Immune Responses
  • Adenosine and Purinergic Signaling
  • Immune Response and Inflammation
  • T-cell and Retrovirus Studies
  • Bacillus and Francisella bacterial research
  • Developmental Biology and Gene Regulation
  • Ethics in Clinical Research
  • T-cell and B-cell Immunology
  • Bacteriophages and microbial interactions
  • COVID-19 Impact on Reproduction
  • RNA regulation and disease
  • Congenital heart defects research
  • Influenza Virus Research Studies
  • Problem and Project Based Learning
  • Innovative Teaching Methods
  • Helminth infection and control

Western University of Health Sciences
2012-2024

Institut National des Sciences Appliquées de Toulouse
2024

Indiana University School of Medicine
2023

Indiana University – Purdue University Indianapolis
2023

Los Angeles City College
2014

University of California, Los Angeles
2006-2010

San Francisco Foundation
2005

Williams (United States)
2005

University of California, San Francisco
2005

Howard Hughes Medical Institute
2001-2002

Type I and type II interferons (IFNs) are cytokines that establish the cellular antiviral state through induction of IFN-stimulated genes (ISGs). We sought to understand basis activity induced by IFNs in relation functions their ISGs. Based on gene expression studies, we systematically identified ISGs performing blinded, functional screens 288 assessed validated these against an RNA virus, vesicular stomatitis virus (VSV), a DNA murine gammaherpes (MHV-68). Overall, 34 elicited effect...

10.1073/pnas.1114981109 article EN Proceedings of the National Academy of Sciences 2012-02-27

Kaposi's sarcoma-associated herpesvirus encodes two transmembrane proteins (modulator of immune recognition [MIR]1 and MIR2) that downregulate cell surface molecules (MHC-I, B7.2, ICAM-1) involved in the infected cells. This downregulation results from enhanced endocytosis subsequent endolysosomal degradation target proteins. Here, we show expression MIR1 MIR2 leads to ubiquitination cytosolic tail their is essential for removal surface. both contain zinc fingers PHD subfamily, these...

10.1083/jcb.200111010 article EN The Journal of Cell Biology 2001-12-24

Little is known about the role of CD1d-restricted T cells in antiviral immune responses. Here we show that lytic replication cycle Kaposi sarcoma–associated herpesvirus (KSHV) promotes downregulation cell-surface CD1d. This caused by expression 2 modulator recognition (MIR) proteins virus, each which loss surface CD1d following transfection into uninfected cells. Inhibition due to ubiquitination α-chain on a unique lysine residue its cytoplasmic tail, triggers endocytosis. Unlike...

10.1172/jci24041 article EN Journal of Clinical Investigation 2005-05-02

Little is known about the role of CD1d-restricted T cells in antiviral immune responses. Here we show that lytic replication cycle Kaposi sarcoma–associated herpesvirus (KSHV) promotes downregulation cell-surface CD1d. This caused by expression 2 modulator recognition (MIR) proteins virus, each which loss surface CD1d following transfection into uninfected cells. Inhibition due to ubiquitination α-chain on a unique lysine residue its cytoplasmic tail, triggers endocytosis. Unlike...

10.1172/jci200524041 article EN Journal of Clinical Investigation 2005-05-02

Abstract Langerhans cells (LC) are a unique subset of dendritic (DC), present in the epidermis and serving as first line defense against pathogens invading skin. To investigate role human LCs innate immune responses, we examined TLR expression function LC-like DCs derived from CD34+ progenitor compared them to peripheral blood monocytes (monocyte-derived DC; Mo-DC). Mo-DCs expressed TLR1–10 mRNAs at comparable levels. Although many TLR-induced cytokine patterns were similar between two cell...

10.4049/jimmunol.177.1.298 article EN The Journal of Immunology 2006-07-01

Abstract The colon is the largest compartment of immune system, with innate cells exposed to antigens in environment. However, mechanisms by which system instigated are poorly defined colorectal cancer (CRC). Here, a population CD16 + neutrophils that specifically accumulate CRC tumor tissues imaging mass cytometry (IMC), fluorescence, and flow cytometry, demonstrated pro‐tumor activity disturbing natural killer (NK) identified. It found these possess abnormal cholesterol accumulation due...

10.1002/advs.202403414 article EN Advanced Science 2024-05-24

Kaposi's sarcoma-associated herpesvirus encodes two related proteins, MIR1 and MIR2, that lead to reduction of the cell surface levels major histocompatibility complex class I other polypeptides involved in immune recognition. MIR2 do not affect assembly or transport their target proteins through secretory pathway; rather, they act enhance selective endocytosis chains from surface. Sequence inspection reveals modulator recognition (MIR) contain an NH2-terminal zinc finger plant homeodomain...

10.1074/jbc.m110265200 article EN cc-by Journal of Biological Chemistry 2002-02-01

Our main objective of this study was to determine how Human Immunodeficiency Virus (HIV) avoids induction the antiviral Type I Interferon (IFN) system. To limit viral infection, innate immune system produces important cytokines such as IFN. IFN set up a critical roadblock virus infection by limiting further replication virus. Usually, production is induced recognition nucleic acids receptors and subsequent downstream signaling. However, importance in defense against viruses has lead most...

10.1371/journal.pone.0137951 article EN cc-by PLoS ONE 2015-09-16

This study investigates the modulation of Type I IFN induction an antiviral state by HIV. IFNs, including IFN-α, are key innate immune cytokines that activate JAK/STAT pathway leading to expression IFN-stimulated genes. gene establishes state, limiting viral infection in IFN-α-stimulated microenvironments. Our previous studies have shown HIV proteins disrupt IFN-α degradation IFN-β promoter stimulator-1, adaptor protein for up-regulation and release into local microenvironment via retinoic...

10.1177/1753425918803674 article EN cc-by-nc Innate Immunity 2018-10-03

Innate immune responses against viral infection, especially the induction of type I interferon, are critical for limiting replication virus. Although it has been shown that DNA can induce to date no natural ligand a virus induces interferon described. Here we screened genome murine gammaherpesvirus 68 with mutations at various genomic locations map region interferon. A repetitive termed 100-base-pair repeat is both necessary and sufficient colinear this in Kaposi's sarcoma-associated...

10.1128/jvi.01718-07 article EN Journal of Virology 2007-12-13

Fragile X Messenger Ribonucleoprotein 1 (FMR1) gene mutations lead to fragile syndrome, cognitive disorders, and, in some individuals, scoliosis and craniofacial abnormalities. Four-month-old (mo) male mice with deletion of the FMR1 exhibit a mild increase cortical cancellous femoral bone mass. However, consequences absence young/aged male/female cellular basis skeletal phenotype remain unknown. We found that results improved properties higher mineral density both sexes 2- 9-mo mice. The...

10.1038/s41413-023-00256-x article EN cc-by Bone Research 2023-05-17

Over the past years, professional students have had extensive exposure to clinical cases during basic science classes. With this in mind, we taken case moment be an opportune time introduce ethics of working with patients biomedical research. Our goal is present a straightforward assignment that allows for active student research into facts Tuskegee Experiment 1900s. The provides necessary background allow student-centered discussion on ethical issues events and ramifications what happened....

10.1128/jmbe.v15i2.781 article EN Journal of Microbiology and Biology Education 2014-12-01

Modulation of innate immunity is critical for virus persistence in a host. In particular, viral-encoded disruption type I interferon, major antiviral cytokine induced to fight viral infection, key component the repertoire pathogenicity genes. We have identified previously undescribed open reading frame within Kaposi's sarcoma-associated herpesvirus (KSHV) genome that encodes homologue human IPS-1 (also referred as MAVS) protein we termed viral-IPS-1 (v-IPS-1). This expressed during lytic...

10.1101/2024.07.24.604690 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2024-07-25

Abstract Various studies have attempted to understand HIV infection under a diverse range of stimulants including cytokine stimulation. Pro-inflammatory cytokines, such as TNF-α, been shown reactivate latency by inducing NF-κB mediated activation the LTR (long terminal repeats) that contain κB transcriptional binding sites. Interferon-alpha (IFN-α), an anti-viral cytokine, is not well studied inducer activation. However, previous work from our group has can block IFN-α signaling in CD4+ T...

10.1101/2024.07.27.605446 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2024-07-28

Morphogenesis and cell-type differentiation are highly coordinated in sensory organs to ensure their function. of the olfactory epithelium (OE) zebrafish provides a unique model study this process as undifferentiated cells aligned around anterior neural plate mature into clusters early neurons across short time scale. While Cxcl12a/Cxcr4b signaling pathway drives process, what constraints on activation apply during morphogenesis unclear. We developed mathematical recapitulating...

10.1101/2024.12.20.629493 preprint EN cc-by-nd bioRxiv (Cold Spring Harbor Laboratory) 2024-12-20
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