Research Bench Lab
Robert Lochhead, PhD

Robert Lochhead, PhD

Assistant Professor; Secondary Faculty in Medicine (Rheumatology)


  • Microbiology & Immunology
    BSB B2855

Contact Information

General Interests

Lyme disease, inflammation and autoimmunity


PhD, Microbiology and Immunology, University of Utah, Salt Lake City, UT, 2014

Research Experience

  • Arthritis, Rheumatoid
  • Autoimmunity
  • Borrelia burgdorferi
  • COVID-19
  • Disease Models, Animal
  • Endothelial Cells
  • Fibroblasts
  • Gene Expression Regulation
  • Host-Pathogen Interactions
  • Inflammation
  • Lyme Disease
  • Lymphocytes

MCW Program / Core Facilities

  • Center for Immunology
  • Center for Infectious Disease Research

Educational Expertise

  • immunology
  • Microbiology

Research Interests

The Lochhead Lab focuses on mechanisms of arthritis pathogenesis, using animal models of Lyme arthritis and clinical samples collected from patients with various types of arthritis. Much of our research focuses on Lyme disease, caused by infection with the tick-borne pathogen Borrelia burgdorferi (Bb). Lyme disease is the most common vector-borne disease in the U.S., and is reaching epidemic levels in many regions, including the Upper Midwest. Lyme disease is an infection-induced multi-system disorder affecting skin (erythema migrans), heart (carditis), joints (arthritis) or neurologic tissue (neuro-borreliosis). Lyme arthritis (LA) is the most common late-stage manifestation of Lyme disease. Although most patients are effectively treated with antibiotics, 10-20% of treated patients develop post-infectious Lyme arthritis, potentially resulting in months or years of disability. Identifying immune factors that contribute to variability in disease severity and treatment outcome is critically important for public health in Lyme-endemic communities such as Wisconsin. By studying LA, we hope to gain important insights into how infection may trigger immune dysregulation, leading to tissue damage, arthritis, and autoimmunity.