School of Medicine
Showing 1-20 of 20 Results
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Carol Clayberger
Professor (Research) of Pediatrics, Emerita
Current Research and Scholarly Interests Our group uses molecular biology, biochemistry, and cellular immunology to investigate the activation and effector function of T lymphocytes. Research in the laboratory is currently focused on three areas: granulysin, a lytic molecule expressed late (7-12 days) after T cell activation; identification of correlates of immunity in diseases such as tuberculosis; and tolerance. The long term goal of this work is to develop new ways to treat human disease.
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Joseph Hernandez
Clinical Assistant Professor, Pediatrics - Immunology and Allergy
Bio I have a research background in basic immunology/biochemistry and animal/cellular models of allergic disease. Since 2016, I have been a full time clinical faculty member caring for patients with a variety of allergic diseases and immune deficiency. I have been involved as a participating clinician and investigator with the PANS clinic at LPCH.
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Alan M. Krensky, M.D.
Shelagh Galligan Professor in the School of Medicine, Emeritus
Current Research and Scholarly Interests Mechanisms and therapies for infection, cancer, autoimmunity and transplantation.
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David B. Lewis
Professor of Pediatrics (Immunology) at the Lucile Salter Packard Children's Hospital
Current Research and Scholarly Interests My laboratory is focused on defining cellular and molecular mechanisms that limit T cell responses to vaccines and pathogens during normal early postnatal development and in cases of inherited genetic immunodeficiencies. We are also determinomg how these limitations in immunity can be overcome by using novel approaches for vaccine adjuvants for influenza vaccine and by using catalytically inactive Cas proteins for inducing endogenous gene expression.
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Elizabeth Amanda Lippner
Clinical Instructor, Pediatrics - Immunology and Allergy
Current Research and Scholarly Interests Schimke Immuno-Osseous Dysplasia (SIOD) is a rare disease that is inherited when children receive two mutated copies of the gene SMARCAL1, one from each parent. SIOD begins in early childhood and causes significant disease, including kidney failure leading to a need for kidney transplantation, stokes, growth delay, cartilage and bone malformations, and recurrent infections due to defects in their immune system. There is currently no cure for children with SIOD. Current therapies only treat the symptoms of the disease; they are not curative and they may not slow or prevent worsening of SIOD. While we know the gene that causes this disease, there are significant knowledge gaps about exactly how mutations in the SMARCAL1 gene lead to problems in so many organs including the kidneys, bones/cartilage, immune system, and vascular system.
As an immunologist, my research lies in better understanding how mutations in SMARCAL1 lead to changes in all of these organs and organ systems, with the ultimate goal of improving treatment options for children with SIOD. T-cell development and function in these children is particularly impaired. In fact, a vast majority of these children develop clinically significant immune deficiency and suffer from recurrent infections by the time they reach mid-childhood. By examining the structure of the SMARCAL1 gene, the protein produced by the SMARCAL1 gene, and the network of other proteins that it interacts with in the t cells of these children, we can better understand the mechanism of disease. These insights into t-cell development and protein expression in patients with SIOD may also enhance our understanding of other t-cell immunodeficiency diseases.
Telomeres are segments of DNA at the end of chromosomes that act as a protective ?cap? against degradation. Each time the cell divides, the telomere sequence is not completely copied, leading to shorter telomere segments with each round of DNA replication. Abnormally shortened telomeres have been associated with aging, cancer, and many other chronic diseases such as diabetes mellitus. This research investigates telomere length maintenance in a disease called Schimke Immuno-Osseous Dysplasia (SIOD). If patients with SIOD have impaired telomere maintenance, then potential therapies targeted at enhancing telomere length/maintenance could be explored. This would open up a whole new area of potential therapy. Additionally, defining the role of SMARCAL1 in telomere maintenance may have general implications for other diseases in which telomere instability has been described, including cancer and diabetes. -
Sean McGhee
Clinical Associate Professor, Pediatrics - Immunology and Allergy
Current Research and Scholarly Interests Bioinformatics
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Rebecca Saenz
Clinical Instructor, Pediatrics - Immunology and Allergy
Current Research and Scholarly Interests Allergy, Immunology, Bioengineering and Biodesign
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Theresa Willett
Clinical Assistant Professor, Pediatrics - Immunology and Allergy
Current Research and Scholarly Interests Clinical research program focusing on children and adolescents with immune-mediated neuropsychiatric symptoms. Research team led by Dr Jennifer Frankovich.
