Estefania Quesada Masachs, M.D., Ph.D.
Research Assistant Professor
Diabetes Research Institute
Department of Medicine, Division of Rheumatology
University of Miami
Seminar Information
Type 1 diabetes (T1D) is an autoimmune disease in which insulin-producing beta cells in pancreatic islets are attacked by the immune system. The classic view is that autoreactive T cells destroy beta cells; however emerging evidence suggests that beta cells actively participate in their own demise through various mechanisms, thus perpetuating the autoimmune response and exacerbating beta cell loss. For instance, under inflammatory stress, beta cells upregulate the expression of HLA class I (a hallmark in T1D histopathology), and HLA class II molecules (which happens to a lesser extend as indicated by recent studies). This enhanced HLA class I and class II expression renders beta cells more susceptible to recognition and destruction by immune T cells. Besides reacting to pro-inflammatory cytokines in their microenvironment, beta cells are capable of producing an array of cytokines and chemokines in response to various stimuli. I will present results from some of our previous studies and key findings in the literature supporting an active role of pancreatic beta cells in T1D. I will discuss the significance of the aforementioned findings, highlight gaps in knowledge within the field, and detail my laboratory's methodological approach to address them. I will present my work leveraging cutting-edge highly multiplexed technology in whole pancreatic tissue sections coupled with a machine learning-based strategy for image analysis, and an in vitro model to study the islet immune attack. This strategy aims at providing a thorough understanding of the pancreas microenvironment and the mechanisms involved in disease initiation and progression.
Dr. Quesada-Masachs received her MD degree at University of Barcelona (UB). She completed the residency in Rheumatology and a 2-year training program in Pediatric Rheumatology at Vall d’Hebron University Hospital (Spain), where she worked as a consultant until early 2018. She did a fellowship at Istituto Giannina Gaslini (Italy), Center of Excellence in Pediatric Rheumatology according to the European League Against Rheumatism (EULAR). Dr Quesada-Masachs completed her PhD in Pediatric Rheumatology at Autonomous University of Barcelona (UAB) with a cum laude and the mention as an international doctor. Her PhD thesis was focused on identifying immunological differences in relation to age and treatment in patients with Juvenile Idiopathic Arthritis. Following her PhD, she joined Prof. von Herrath’s lab, at La Jolla Institute for Immunology (California) as a post-doctoral fellow, where she focused on studying the role that different immune cells, cytokines and other signaling molecules play in disease initiation and progression in autoimmune type 1 diabetes (T1D). During that time, she contributed to solve a long-standing controversy in the type 1 diabetes (T1D) field, demonstrating that beta cells can upregulate HLA class II expression in T1D and in vitro after receiving inflammatory stimulus. Following her appointment as an instructor at la Jolla Institute for Immunology, Dr Quesada-Masachs was awarded with an R01 and, in 2023, was recognized by the Network for Pancreatic Organ Donors with Diabetes (nPOD) with the Young Investigator of the Year Award. Currently she has position as Research Assistant Professor at the Diabetes Research Institute and the University of Miami, where she investigates the mechanisms involved in T1D initiation and progression. In her studies, she uses state of the art microscopy technology and software to obtain and analyze high resolution images from human pancreatic tissues and 3D islet and organoid structures. In another related area of her research, she is applying this cutting-edge technology to investigate human synovial tissue of patients affected by chronic inflammatory arthritis. Dr. Quesada-Masachs has a multidisciplinary background, and she is particularly interested in studying autoimmune diseases that typically start in childhood and younger individuals, such as T1D and juvenile idiopathic arthritis.