SLB @ AAI 2019 announced |
SLB Speakers @ AAI 2019 announcedSLB is pleased to host yet another guest symposium. In 2019, SLB will host a session at the AAI 2019 meeting in San Diego, CA. Below are the featured speakers that have been selected from applications from the membership. Another example of the many opportunities that SLB membership offers!
Dr. Noah Fine completed his Masters degree at York University with Dr. Ron Pearlman studying siRNA induced silencing in the single celled protozoan, Tetrahymena thermophila. This work, published in Cell, was listed as part of the number one scientific breakthrough of 2002 in Science Magazine (J. Couzin, 2002). From here, Dr. Fine did his doctoral studies with Dr. Rob Rottapel at the University of Toronto, focusing on the mechanosensory response of neutrophils to shear stress due to blood flow. This work demonstrated a unique role of the guanine nucleotide exchange factor, GEF-H1, for neutrophil mechanosensory responses and efficient recruitment to inflamed tissues. Dr. Fine is currently doing his Post-Doctoral studies with Dr. Michael Glogauer in the department of Dentistry at UofT. Motivated by the highly sensitive nature of neutrophils towards extracellular stimuli, he developed a novel flow cytometric assay for assessing the basal immunophenotype of neutrophils in biological fluids. Through this approach Dr. Fine has demonstrated unique neutrophil activation/priming states at high resolution in blood and saliva of both mouse and human. The primary goal of his ongoing studies is to identify changes in tissue and systemic neutrophil activation states in health and during acute and chronic inflammation, with the goal of developing sensitive diagnostic and prognostic clinical applications. Dr. Lee is an Assistant Professor in the Departments of Ophthalmology, and Microbiology and Immunology at the University of Oklahoma Health Sciences Center. His interest is in autoimmune disease of the eye, autoimmune uveoretinitis. A mouse model of human autoimmune uveitis, experimental autoimmune uveitis (EAU) has been used to better understand the mechanisms of this blinding disease. In contrast to chronic human uveitis, EAU resolves without intervention and mice are resistant to recrudescence of uveitis because of regulatory immunity found in the spleen. This regulatory immunity requires post-EAU Treg cells to be activated by post-EAU antigen presenting cells (APC). We have shown that the melanocortin 5 receptor (MC5r) is required for the emergence of a suppressive APC in the post-EAU spleen, and this APC is a source of adenosine that activates the post-EAU Treg cell through the adenosine 2A receptor (A2Ar). This is an interesting finding, because these two pathways have been shown to individually regulate immunity, but our observation is the first to link the two pathways. The result of stimulating this melanocortin-adenosinergic pathway is an autoantigen specific Treg cell that suppresses EAU. Dr. Lee's focus is how these Treg cells function to suppress inflammation, the intracellular signaling pathway that occur in the suppressor APC upon MC5r stimulation, and to determine if MC5r or A2Ar stimulation is effective in the promotion of regulatory activity in uveitis patients.
Dr. Allison Malloy is an Assistant Professor in the Department of Pediatrics at the Uniformed Services University of the Health Sciences in Bethesda, Maryland. Her research program focuses on the influence of age-dependent immune development in response to respiratory viruses, primarily respiratory syncytial virus and influenza. Her interest in early life immunity to infection was influenced by her experiences as a resident at the Children’s Hospital of Philadelphia, which was followed by a Pediatric Infectious Disease Fellowship at Children’s National Medical Center in Washington, DC. During Fellowship, she worked in the laboratory of Dr. Barney Graham at the Vaccine Research Center, NIAID, NIH and developed model systems for studying neonatal immunity in the respiratory tract. The long-term goals of her research program are to target infant dendritic cell activation to induce effective memory T cell differentiation for intelligent vaccine design. |