Immunology and Microbiology: Faculty Directory

Matthew Pipkin

Matthew Pipkin Ph.D.

Associate Professor
Phone: (561) 228-2182
Mailing Address:
Location C243
130 SCRIPPS WAY BLDG, 2C2
JUPITER FL 33458
Research Summary:

The overall focus of the Pipkin lab is to elucidate how chromatin structure and transcription controls the gene expression programs that establish and maintain the differentiated states of T cells. The lab specifically studies how naïve CD8 T cells differentiate into effector and memory cytotoxic T lymphocytes (CTL). CTL are killer lymphocytes that hold outstanding promise for controlling viral infections and cancer therapeutically, as they can be employed in adoptive immunotherapy and are the target of successful vaccination. The Pipkin lab has developed novel approaches to map the fundamental repeating structures of chromatin (nucleosomes) at unprecedented resolution, novel reporter genes to track cells in vivo that induce expression of Prf1, an essential gene that is required for the anti-tumor killing activity of CTL, and the only systems to conduct genome-scale pooled RNAi screens in T cells, in vivo, during the course of actual viral infections. Using these tools and approaches, the Pipkin lab is clarifying how transcription factors govern the specific organization of nucleosomes that enforces CTL differentiation, identifying the chromatin regulatory factors that maintain the differentiated state epigenetically, and demonstrating how these processes mediate durable immunity.

Publications:
Education:
  • 2005
    Ph.D. in Microbiology and Immunology
    University of Miami, School of Medicine
  • 1998
    Bachelor's of Science in Microbiology and Immunology
    University of Miami
Laura Solt

Laura Solt Ph.D.

Associate Professor
Phone: (561) 228-2295
Mailing Address:
Location C227
130 SCRIPPS WAY BLDG 3C1
JUPITER FL 33458

Laura A. Solt, Ph.D., is an Associate Professor in the Department of Immunology and Microbiology at Scripps Florida in Jupiter, Florida. She received her B.A. from Boston College and her Ph.D. in Immunology from the University of Pennsylvania. After completing her postdoctoral research at Scripps, she started her independent laboratory at Scripps Florida in 2013. Dr. Solt’s research is focused on understanding the biological roles of nuclear receptors in the immune system, with a specific focus on Th17 cells, and how their expression, function, and activity affects disease. Her lab uses a combination of molecular biology, genetic, and chemical biology approaches coupled with mouse models of autoimmunity and chronic inflammation to study the RORs, REV-ERBs, and NR2F6 either individually and/or cross-talk between the receptors. As ligand-regulated transcription factors, nuclear receptors function as excellent targets for the treatment of a variety of diseases. Therefore, we also work in close collaboration with medicinal chemists to design and develop small molecule ligands to these receptors to further probe their functions in vitro, in vivo, and to evaluate their therapeutic potential. Using these approaches, we described a negative regulatory role for the nuclear receptor REV-ERBa in Th17 cell development and autoimmunity. We also described the design and synthesis of newer, more potent synthetic REV-ERB modulators that target Th17 cells in vivo. Recently, we have extended our studies to better understand how heme, the REV-ERBs endogenous ligand, regulates REV-ERB activity in Th17 cells. Finally, we also described the design and synthesis of synthetic RORa modulators. We published a role for RORa in Th17 cells and the characterization of RORa-selective small molecules to target Th17 cells and treat Th17-mediated autoimmunity. Targeting the REV-ERBs or RORa demonstrate an alternative approach to the current design of RORgt modulators – of which many have entered clinical trials and failed for numerous reasons. Insight into the transcriptional regulation of nuclear receptors and their ligand(s) function is essential to comprehend the signaling pathways that govern Th17 cell homeostasis vs. pathogenicity as well as the rational design of therapeutics for specific disease indications.

Accomplishments:
  • Ruth L. Kirschstein National Research Service Awards
    2010-2013 · National Institutes of Health
Research Summary:

The underlying theme of the research performed in the Solt laboratory is to understand the biologically relevant roles of nuclear receptors, a superfamily of ligand regulated transcription factors, in the immune system. Our lab uses a combination of molecular biology, genetic, and chemical biology approaches coupled with mouse models of autoimmunity and chronic inflammation to study how different nuclear receptors’ expression, function, and activity affects disease. As ligand-regulated transcription factors, nuclear receptors are excellent therapeutic targets for the treatment of a variety of diseases. Therefore, we also work in collaboration with medicinal chemists to develop small molecule ligands to these receptors to further probe their function in vitro and in vivo. Each receptor is unique and can have ligand- and/or tissue-specific effects. Thus, we aim to gain a better understanding of nuclear receptor activity in tissue and disease-specific contexts to determine their therapeutic potential and for more rational drug design.

Research Interests:
  • Autoimmune Disease
  • Cancer Immunotherapy
  • Immunometabolism
  • Mucosal immunology
  • Neuroimmunology
Publications:
Education:
  • 2009-2013
    Postdoctoral Fellow
    The Scripps Research Institute – Florida
  • 2008
    Ph.D. in Immunology
    University of Pennsylvania
  • 1998
    Bachelor's of Science in Psychology
    Boston College
Susana Valente

Susana Valente Ph.D.

Professor And Chair, Department Of Immunology And Microbiology
Phone: (561) 228-3454
Mailing Address:
Location C329
130 SCRIPPS WAY BLDG 3C1
Jupiter FL 33458
Accomplishments:
  • NIAID MERIT Award.
    2022 · Host factors regulating HIV latency and reactivation.
  • Co-leader of HOPE (HIV Obstruction by Programmed Epigenetics) – Martin Delaney Collaboratory for HIV Cure (UM1)
    2021-current · NIH
  • Founder
    2019-Current · Thimble Therapeutics
  • Editorial Board
    2018-Current · Retrovirology
  • Editorial Board
    2018-Current · Viruses
  • Permanent member NIH- ADDT and HVCD study sections
    2014-2020 · NIH-NIAID
  • Early Career Reviewer (ECR) program
    2012-2013 · NIH-NIAID
  • Landenberger Foundation Award for early career investigators
    2010-2012 · Landenberger Foundation
  • Research Scholar Development Award (K22)
    2009-2011 · NIAID
  • Awarded
    2008 · NIAID Career Transition Award (K22)
  • Awarded
    2007-2008 · Portuguese Ministry of Education Fellowship
  • Awarded
    2005-2007 · American Foundation AIDS Research (amfAR) Fellowship
  • Awarded
    1998-2002 · Portuguese Ministry of Education Scholarship
Research Summary:

According to the latest statistics published by the UNAIDS/WHO in 2021, 38.4 million people were living with the Human Immunodeficiency Virus (HIV), and 40.1 million have died as a result of HIV. Although antiretroviral drugs have had a dramatically beneficial impact on HIV-infected individuals who have access to treatment, they have had a negligible impact on the global epidemic. Therapies for retroviral infections now used in clinical practice have limitations in that they often only shorten the duration of disease symptoms but fail to completely eradicate the virus with viral replication and disease recurring after discontinuation of the drug therapy. Additionally, the emergence of HIV variants with drug-resistance is an ongoing clinical problem. Clearly having a larger repertoire of therapeutic agents would be beneficial for combating the HIV epidemic.

Retroviruses, due to their limited genome size and content, require the assistance of multiple host cellular proteins at each step in their elaborate replication cycle. Host cells, in response, have evolved many mechanisms for inhibiting viral replication. We have taken a general approach to identify the molecular interactions occurring within a cell that are critical for viral replication, or genes that have evolved in mammalian cells to regulate viral replication. The discovery of cellular factors involved in retroviral replication and our increased knowledge of their mode of action may leverage novel antiviral approaches in clinical settings as one could block the modified use without affecting cell viability.

Publications:
Education:
  • 2009
    Postodoctoral fellow
    Columbia University, NYC
  • 2002
    Ph.D. Microbiology-Virology
    University of Paris Diderot (Paris VII)
  • 1998
    Master's of Science in Biotechnology
    De Montfort University
  • 1997
    Master's of Science in Maîtrise Biochemistry
    University of Paris Diderot (Paris VII)
  • 1996
    Bachelor's of Science in Applied Chemistry and Biotechnology
    New University of Lisbon
Mauricio Martins

Mauricio Martins Ph.D.

Associate Professor
Phone: (561) 228-3051
Mailing Address:
Location C221
130 SCRIPPS WAY BLDG, 2B2
JUPITER FL 33458
Accomplishments:
  • Vaccine’s Young Investigator
    2016 ·
Research Summary:

I am interested in developing practical immune interventions against globally relevant human pathogens. HIV is the current topic of my research. My group is using rhesus macaque models of HIV/AIDS to develop active and passive immunization strategies for preventing and treating HIV infection.

Publications:
Corinne Lasmézas

Corinne Lasmézas Ph.D.

Professor
Phone: (561) 228-3456
Mailing Address:
Location B213
130 SCRIPPS WAY BLDG, 2B2
JUPITER FL 33458
Research Summary:

Neurodegenerative diseases

Our laboratory focuses on the study of neurodegenerative diseases, especially those linked to protein misfolding (protein misfolding neurodegenerative diseases, or PMNDs). These diseases comprise Alzheimer’s, Parkinson’s, Huntington’s, prion diseases, fronto-temporal dementia, and amyotrophic lateral sclerosis. None of them are curable. They are all due to host proteins loosing their natural, functional conformation and adopting a new shape that renders them neurotoxic and prone to aggregation.

Prion diseases constitute the prototypic PMND. These rapidly fatal neurodegenerative diseases affect humans and animals and are caused by infectious aggregates of the prion protein PrP, called prions. In humans, prions cause Creutzfeldt-Jakob disease. In animals, the recent epidemic of bovine spongiform encephalopathy in the United Kingdom has caused major turmoil throughout Europe, and later, in other countries such as Japan, Canada and the United States, because the bovine prion disease is transmissible to humans causing variant Creutzfeldt-Jakob disease. The transmissibility of the latter by blood transfusion created a novel public health issue.

Alzheimer’s and Parkinson’s diseases affect 5.8 and 1 Million people in the USA, respectively. Their incidence has steadily increased with an aging population, having a major impact on public health, society and the economy. Alzheimer’s disease is the 6th leading cause of death in developed countries. Amyotrophic lateral sclerosis (ALS or Lou Gehrig’s disease) is an orphan disease causing a progressive muscle weakness and paralysis, affecting an estimated 30,000 people in the USA.

In recent years, it has been discovered that aggregates of amyloidogenic proteins such as Ab, tau, a-synuclein or SOD-1 involved in Alzheimer’s, Parkinson diseases and amyotrophic lateral sclerosis, respectively, spread from cell to cell in culture and in the living organism similarly to PrP aggregates, showing “prion-like” behavior. There are other features common to these toxic proteins and the way they injure neurons (e.g. toxicity of low molecular weight aggregates, impairment of protein degradation mechanisms such as autophagy, mitochondrial distress).

Our aim is the development of novel, disease-modifying therapeutic approaches for protein misfolding neurodegenerative diseases. We think that this aim will be best achieved by intervention strategies based on targeting toxic protein aggregates, and blocking the neurodegenerative process to achieve neuroprotection. We are pursuing these goals by studying the underlying biology, defining therapeutic targets, identifying active molecules by high-throughput screening and developing lead compounds. The latter two tasks are performed in collaboration with our lead identification and chemist colleagues on campus.

Publications:
Education:
  • 1995
    Ph.D. in Neurosciences
    Pierre and Marie Curie University
  • 1993
    Doctor of Veterinary Medicine
    University of Toulouse, Toulouse National Veterinary School
  • 1992
    Master's of Science in Neurosciences
    Pierre and Marie Curie University
  • 1990
    Diploma in Aeronautic and Space Medicine
    University of Toulouse, University of Medicine