Dr. Robert Colbert is a board certified pediatric rheumatologist with a long-standing interest in understanding the pathogenesis of spondyloarthritis. After completing clinical training in pediatrics and rheumatology, he did postdoctoral research in molecular immunology at the University of North Carolina. From there he joined the faculty at Cincinnati Children’s Hosptial Medical Center and the University of Cincinnati, where he became Professor of Pediatrics and chief of the Divison of Rheumatology. He joined the NIAMS Intramural Research Program in 2008 as Chief of the Pediatric Translational Research Branch.

Research Statement

The Pediatric Translational Research Branch is focused on understanding the etiology and pathogenesis of early onset arthritis, including axial disease in juvenile spondyloarthritis. Patients are studied under a natural history protocol (#11-AR-0223; Studies on the Natural History and Pathogenesis of Spondyloarthritis) to find better clinical, laboratory, and imaging modalities to define axial involvement and disease outcome. We are particularly interested in genetic contributions to early onset axial disease. The laboratory also utilizes animal models to understand the role of risk genes and how they interact, and dissect molecular mechanisms that drive arthritis and spondyloarthritis pathogenesis. Current studies are focused on defining novel effects of ERAP1 on HLA-B27, the role of endoplasmic reticulum quality control pathways in HLA-B27 misfolding, and how misfolding impacts immune function. We also have studies addressing the role of gut microbiota in experimental spondyloarthritis.

Scientific Publications

Novel Inter-omic Analysis Reveals Relationships Between Diverse Gut Microbiota and Host Immune Dysregulation in HLA-B27-Induced Experimental Spondyloarthritis.

Gill T, Brooks SR, Rosenbaum JT, Asquith M, Colbert RA
Arthritis & rheumatology (Hoboken, N.J.).
2019 Nov;
doi: 10.1002/art.41018
PMID: 31216122

The Role of Autophagy in the Degradation of Misfolded HLA-B27 Heavy Chains.

Navid F, Layh-Schmitt G, Sikora KA, Cougnoux A, Colbert RA
Arthritis & rheumatology (Hoboken, N.J.).
2018 May;
doi: 10.1002/art.40414
PMID: 29342507

Germline gain-of-function myeloid differentiation primary response gene-88 (MYD88) mutation in a child with severe arthritis.

Sikora KA, Bennett JR, Vyncke L, Deng Z, Tsai WL, Pauwels E, Layh-Schmitt G, Brundidge A, Navid F, Zaal KJM, Hanson E, Gadina M, Staudt LM, Griffin TA, Tavernier J, Peelman F, Colbert RA
The Journal of allergy and clinical immunology.
2018 May;
doi: 10.1016/j.jaci.2018.01.027
PMID: 29427642

Effects of HLA-B27 on Gut Microbiota in Experimental Spondyloarthritis Implicate an Ecological Model of Dysbiosis.

Gill T, Asquith M, Brooks SR, Rosenbaum JT, Colbert RA
Arthritis & rheumatology (Hoboken, N.J.).
2018 Apr;
doi: 10.1002/art.40405
PMID: 29287307

ERAP1 reduces accumulation of aberrant and disulfide-linked forms of HLA-B27 on the cell surface.

Tran TM, Hong S, Edwan JH, Colbert RA
Molecular immunology.
2016 Jun;
doi: 10.1016/j.molimm.2016.04.002
PMID: 27107845

Identification of Interleukin-1β-Producing Monocytes That Are Susceptible to Pyronecrotic Cell Death in Patients With Neonatal-Onset Multisystem Inflammatory Disease.

Edwan JH, Goldbach-Mansky R, Colbert RA
Arthritis & rheumatology (Hoboken, N.J.).
2015 Dec;
doi: 10.1002/art.39307
PMID: 26245468


Boston University
B.A., Chemistry and Biology, Summa Cum Laude

University of Vermont
M.S., Biochemistry

Medical Scientist Training Program, University of Rochester School of Medicine.
M.D., Ph.D.


Pediatrics, Strong Memorial Hospital at the University of Rochester

Pediatric Rheumatology, Duke University and the University of North Carolina

Last Updated: March 2020