Hideki Ueno, MD, PhD
- PROFESSOR | Microbiology
Research Topics:Autoimmunity, B Cells, Cellular Differentiation, Cellular Immunity, Cytokines, Dendritic Cells, Immunology, Infectious Disease, Inflammation, Influenza Virus, Lymphocytes, Molecular Biology, Neuroscience, T Cells
Hideki Ueno, M.D, Ph.D. is a Professor at Global Health and Emerging Pathogens Institute and Department of Microbiology. Dr. Ueno has more than 15 years of experience on immunology research with primary human cells. His research focuses on the studies on the adaptive immune system in humans, the major immunological protection mechanism in charge of generation and maintenance of antigen-specific immune response.
The Ueno Lab webpage: http://labs.icahn.mssm.edu/uenolab/
Multi-Disciplinary Training AreasImmunology [IMM], Microbiology [MIC]
MD, Kyoto University
PhD, Graduate School of Medicine, Kyoto University
Post-doctoral fellow, Baylor Institute for Immunology Research
Basic Science on Human T follicular helper cells
T follicular helper (Tfh) cells represent a CD4+ T cell subset specialized for providing help to B cells. Dysregulation of Tfh responses are associated with autoimmunity (when excessive) and with poor antibody response (when insufficient). My lab aims to identify the molecules and pathways controlling human Tfh responses.
Immune Mechanisms Associated with Protective Ab Response for Influenza
While both vaccination and infection induce Tfh and antibody response, the magnitude and the quality of Tfh responses are radically different. Our previous studies show that seasonal influenza vaccination induces antibody response by activating a specific Tfh subset, called Tfh1 cells, together with influenza-specific memory B cells in humans. We aim to define the fundamental biological differences on memory Tfh cells generated by influenza infection and vaccination, and determine the key molecules and pathways associated with long-lived memory Tfh cells in humans.
T Follicular Helper Cells in Human Autoimmunity
Tfh cells play a major pathogenic role in Systemic Lupus Erythematosus (SLE). However, the precise mechanism remains largely obscure. We are aiming at identifying the feature of pathogenic Tfh cells unique to SLE, and determining how the pathogenic Tfh cells contribute to altered B cell responses in patients with SLE.
Pathogenic CD4+ T cells in Human Neuroinflammatory Diseases
Depletion of B cells is effective to treat patients with neuromyelitis optica (NMO) and multiple sclerosis (MS), but the immune mechanism remains unclear. We are interested in how B cell depletion affects the antigen-specific CD4+ T cell repertoires in patients. Towards this goal, we are currently developing a new assay that permits the detection of antigen-specific T cells with superior sensitivity and specificity to currently available assays.