- Inman RD, Chiu B. Heavy metal exposure reverses genetic resistance to Chlamydia-induced arthritis. Arthritis Res Ther 11:19, 2009.
- Bharhani MS, Chiu B, Inman RD. Natural Killer T cells define outcomes in experimental reactive arthritis. Internat Immunol 21: 859-870, 2009.
- Tsui FWL, Haroon N, Reveille JD, Rahman P, Chiu B, Tsui HW, Inman RD. Association of an ERAP1 ERAP2 haplotype with familial ankylosing spondylitis. Ann Rheum Dis 69:733-736, 2010.
- Gracey E, Inman RD. Chlamydia-induced ReA: immune imbalances and persistent pathogens. Nat Rev Rheumatol 8: 55-59, 2011.
- Las Heras F, DaCosta RS, Pritzker KPH, Haroon N, Netchev GPH, Tsui HW, Chiu B, Erwin M, Tsui FWL, Inman RD. Aberrant axial mineralization precedes spinal ankylosis in ank/ank mice: a molecular imaging study. Arthritis Res Ther 13:R163, 2011.
- Danoy P, Pryce K, Hadler J, Bradbury LA, Farrar C, Pointon J, Australo-Anglo-American Spondyloarthritis Consortium (TASC), Ward M, Weisman M, Reveille JD,Wordsworth BP, Stone MA, Maksymowych WP, Rahman P, Gladman D, Inman RD, Brown MA. Association of variants at 1q32 and STAT3 with ankylosing spondylitis suggests genetic overlap with Crohn's disease. PLoS Genet 7: 101371, 2011.
- Akram A, Inman RD. Immunodominance: a pivotal principle in host response to viral infections. Clin Immunol 143: 99-115, 2012.
- Inman RD, Chiu B. Nafamostat mesylate, a serine protease inhibitor, demonstrates novel antimicrobial properties and effectiveness in Chlamydia-induced arthritis. Arthritis Res Ther. 14:R150, 2012.
- Haroon N, Tsui, F, Uchanska-Ziegler B, Ziegler, A, Inman RD. Endoplasmic Reticulum Aminopeptidase 1 (ERAP1) exhibits functionally significant interaction with HLA B27 and relates to subtype specificity in ankylosing spondylitis. Ann Rheum Dis 7:589-595, 2012
The broad research themes in my lab have been the interaction of infection and autoimmunity, and the environmental-genetic interplay in the pathogenesis of arthritis. This has encompassed translational research into the immunobiology of spondylitis and related forms of arthritis, animal models of infection-induced arthritis and autoimmunity, and the cell biology of host:pathogen interactions.