Laura Campisi

ORCID: 0000-0003-4173-4521
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About
Contact & Profiles
Research Areas
  • Immunotherapy and Immune Responses
  • T-cell and B-cell Immunology
  • interferon and immune responses
  • Immune Response and Inflammation
  • Amyotrophic Lateral Sclerosis Research
  • Immune Cell Function and Interaction
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Cancer therapeutics and mechanisms
  • Diabetes and associated disorders
  • Virus-based gene therapy research
  • Chromosomal and Genetic Variations
  • RNA Research and Splicing
  • HIV Research and Treatment
  • Immune cells in cancer
  • RNA modifications and cancer
  • Influenza Virus Research Studies
  • Psoriasis: Treatment and Pathogenesis
  • CRISPR and Genetic Engineering
  • Pancreatic function and diabetes
  • Protein Degradation and Inhibitors
  • Respiratory viral infections research
  • Prion Diseases and Protein Misfolding
  • RNA Interference and Gene Delivery
  • Cell Adhesion Molecules Research
  • Cell death mechanisms and regulation

Icahn School of Medicine at Mount Sinai
2012-2023

Université Côte d'Azur
2007-2011

Inserm
2007-2011

Centre d'Immunologie et des Maladies Infectieuses
2007-2011

Fondation de l'Avenir
2011

Institut de Pharmacologie Moléculaire et Cellulaire
2007-2009

Brookhaven National Laboratory
1994

CX3CR1 expression is associated with the commitment of CSF-1R+ myeloid precursors to macrophage/dendritic cell (DC) lineage. However, relationship CX3CR1+ macrophage/DC precursor (MDP) other DC and role in macrophage development remain unclear. We show that MDPs give rise conventional DCs (cDCs), plasmacytoid (PDCs), monocytes, including Gr1+ inflammatory monocytes differentiate into TipDCs during infection. deficiency selectively impairs recruitment blood spleen after transfer acute...

10.1084/jem.20081385 article EN The Journal of Experimental Medicine 2009-03-09

Unwinding DNA and unleasing inflammation Fighting infections often comes with collateral damage, which sometimes can be deadly. For instance, in septic shock, the overwhelming release of inflammatory mediators drives multi-organ failure. Rialdi et al. now report a potential new therapeutic target for controlling excessive inflammation: unwinding enzyme topoisomerase I (Top1) (see Perspective by Pope Medzhitov). Upon infection, Top1 specifically localizes to promoters pathogen-induced genes...

10.1126/science.aad7993 article EN Science 2016-04-29

Cytolysis, interferon γ and tumor necrosis factor (TNF) α secretion are major effector mechanisms of memory CD8+ T cells that believed to be required for immunological protection in vivo. By using mutants the intracellular bacterium Listeria monocytogenes, we found none these activities is sufficient protect against secondary infection with wild-type (WT) bacteria. We demonstrated CCL3 derived from reactivated efficient killing WT induces a rapid TNF-α by innate inflammatory mononuclear...

10.1084/jem.20070204 article EN The Journal of Experimental Medicine 2007-08-13

The penton base gene from adenovirus type 12 (Ad12) was sequenced and encodes a 497-residue polypeptide, 74 residues shorter than the Ad2. Ad2 Ad12 proteins are highly conserved at amino- carboxy-terminal ends but diverge radically in central region, where 63 missing sequence. Conserved within this variable region is sequence Arg-Gly-Asp (RGD), which, base, binds to integrins target cell membrane, enhancing rate or efficiency of infection. expressed Escherichia coli, purified refolded...

10.1128/jvi.68.9.5925-5932.1994 article EN Journal of Virology 1994-09-01

ABSTRACT Endogenous retroviruses (ERVs) occupy extensive regions of the human genome. Although many these retroviral elements have lost their ability to replicate, those whose insertion took place more recently, such as HML-2 group HERV-K elements, still retain intact open reading frames and capacity produce certain viral RNA and/or proteins. Transcription ERVs is, however, tightly regulated by dedicated epigenetic control mechanisms. Nonetheless, it has been reported that some pathological...

10.1128/jvi.01507-17 article EN Journal of Virology 2017-10-19

RNA viruses are a major human health threat. The life cycles of many highly pathogenic like influenza A virus (IAV) and Lassa depends on host mRNA, because viral polymerases cleave 5′-m7G-capped transcripts to prime mRNA synthesis ("cap-snatching"). We hypothesized that start codons within cap-snatched could generate chimeric human-viral mRNAs with coding potential. report the existence this mechanism gene origination, which we named "start-snatching." Depending reading frame,...

10.1016/j.cell.2020.05.035 article EN cc-by Cell 2020-06-01

Endogenous retroviruses (ERVs) are remnants of ancient parasitic infections and comprise sizable portions most genomes. Although epigenetic mechanisms silence ERVs by generating a repressive environment that prevents their expression (heterochromatin), little is known about silencing residing in open regions the genome (euchromatin). This particularly important during embryonic development, where induction repression distinct classes occur short temporal windows. Here, we demonstrate...

10.1016/j.molcel.2023.10.036 article EN cc-by Molecular Cell 2023-11-22

Abstract Memory CD8 + T lymphocytes are critical effector cells of the adaptive immune system mediating long‐lived pathogen‐specific protective immunity. Three signals – antigen, costimulation and inflammation orchestrate optimal T‐cell priming differentiation into memory shape functional fate ability to protect against challenge infections. While among conventional spleen DCs (cDCs), CD8α but not − cDCs most efficiently mediate priming, it is unclear which subset, irrespective their...

10.1002/eji.201041036 article EN European Journal of Immunology 2011-03-16

The SecA2 auxiliary secretion system of Gram-positive bacteria promotes the export virulence proteins essential for colonization host in case both Mycobacterium tuberculosis and Listeria monocytogenes, two intracellular causing diseases humans. We others have demonstrated that this is also linked to onset long-term CD8(+) T cell-mediated protective immunity mice. In L. expression inside cytosol infected cells correlates with generation CCL3-secreting memory are required protection against...

10.1128/iai.00020-11 article EN Infection and Immunity 2011-03-15

ABSTRACT Type 1 diabetes (T1D) affects a genetically susceptible population that develops autoreactive T cells attacking insulin-producing pancreatic β cells. Increasingly, neoantigens are recognized as critical drivers of this autoimmune response. Here, we report novel insulin neoepitope generated via post-translational cysteine-to-serine conversion (C>S) in human patients, which is also seen the autoimmune-prone non-obese diabetic (NOD) mice. This modification driven by oxidative stress...

10.1101/2024.11.07.622538 preprint EN 2024-11-11

SUMMARY The ongoing pandemic caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) is currently affecting millions of lives worldwide. Large retrospective studies indicate that an elevated level inflammatory cytokines and pro-inflammatory factors are associated with both increased disease severity mortality. Here, using multidimensional epigenetic, transcriptional, in vitro vivo analyses, we report Topoisomerase 1 (Top1) inhibition suppresses lethal inflammation induced...

10.1101/2020.12.01.404483 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2020-12-01

Antigen presenting cells (APC) are able to process and present T antigens from different origins.This mechanism is highly regulated, in particular by Patter Recognition Receptor (PRR) signals.Here, I detail a protocol designed assess vitro the capacity of APC derived bacteria, apoptotic infected cells.

10.21769/bioprotoc.2307 article EN BIO-PROTOCOL 2017-01-01

Abstract Amyotrophic Lateral Sclerosis (ALS) is a heterogeneous neurodegenerative disorder that affects motor neurons in the brain and spinal cord, causing progressive loss of voluntary muscle control1,2. ALS heterogeneity includes age manifestation, rate progression, anatomical sites symptom onset. In addition, disease-causing mutations specific genes have been identified are used to catalog different subtypes ALS3. Interestingly, several ALS-associated shown affect immune functions,...

10.21203/rs.3.rs-798338/v1 preprint EN cc-by Research Square (Research Square) 2021-08-14
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