NIH/NIAID, "Brucella Survival Strategy Requires Endoplasmic Reticulum Restructuring and Interferes with Innate Immunity," (2016-2020). Smith, Co-Investigator/Subaward Principal Investigator
NIH-NIEHS, “Pathogenic studies in families with twins or siblings discordant for systemic rheumatic disorders” (2011-ongoing). Smith, Site PI
NIH-NIAID and Federal University of Minas Gerais (R01 AI116453), “Brucella survival strategy requires endoplasmic reticulum restructuring and interferes with innate immunity” (2015-2020). Smith, Co-Investigator
NIH-NHLBI (P01 HL070831), “COAST - rhinovirus infection and asthma in children and adolescents” (2011-2018). Smith, Project I Co-Investigator
National Institutes of Health - National Institute of Allergy and Infectious Diseases
The goal of this project is to determine the role of the host macrophage UPR in supporting Brucella replication in vitro and in vivo in a murine model.
National Patient Safety Foundation
The project identified strategies that address common barriers and facilitators of family engagement during bedside rounds, using established human factors and systems engineering approaches. The information gained from this project will be used to develop system-wide interventions to improve family engagement in bedside rounds.
NIH-NIAID (R01 AI073558), “Brucella epitope recognition by CD8+ t cells” (2012-2017). Smith, Co-PI
NIH/UW ICTR, "Development of IL-17 Targeting Small Molecule Therapeutics for Autoimmune Diseases" (2015-2016). Smith, Principal Investigator
Rheumatology Research Foundation, “Analysis of causal variants in the IL-23/IL-17 pathway” (2013-2015). Smith, PI
NIH-NIAID and University of Chicago (U54 IA057153), “The role of the host unfolded protein response in Brucella replication” (2013-2014). Smith, Subaward PI
University of Wisconsin Graduate School, “The role of the host unfolded protein response in Brucella replication” (2013-2014). Smith, PI
American College of Rheumatology Research Foundation
Pilot grant award to compare cytokine responses and underlying biochemical signaling in macrophages from ankylosing spondylitis and spondyloarthritis patients.
Arthritis National Research Foundation, “Excess IL-23 production and underlying mechanisms in macrophages from ankylosing spondylitis patients” (2011-2012). Smith, PI
University of Wisconsin Graduate School, “The interaction of IFN-beta and endoplasmic reticulum stress in mediating hepatic ischemia reperfusion injury” (2011-2012). Smith, PI
NIH-NIAID (K08 AI081045), “Regulation of IFN-β induction by P2X7 purinergic receptor signaling” (2009-2012). Smith, PI
Novartis, “CACZ885D2306 An open-label, long-term safety and efficacy study of ACZ885 (anti-interleukin-1b monoclonal antibody) administered for at least 6 months in patients with the following cryopyrin-associated periodic syndromes: familial cold autoinflammatory syndrome, muckle-wells syndrome, or neonatal onset multisystem inflammatory disease” (2008-2011). Smith, Site PI
NIH-NCRR (UL1 RR025011), “ER stress and cytokine regulation” (2008-2009). Smith, KL2 Scholar
University of Wisconsin Graduate School, “An investigation of the interaction between the unfolded protein response, HLA-B27 and inflammatory cytokine production in macrophages” (2008-2009). Smith, PI
NIH-NCRR (UL1 TR025011), “ER Stress and cytokines in ankylosing spondylitis” (2008-2009). Smith, Pilot Grant PI
Arthritis Foundation (post-doctoral fellowship), “HLA-B27 misfolding and cytokine regulation” (2004-2007). Smith, PI