Rheumatology and Autoimmunity
The Rheumatology and Autoimmunity group is focused on determining how self-reactive immune cells develop, persist and cause severe pathology in patients with rheumatic autoimmune disease. The purpose of this research is to uncover more specific therapeutic targets that can be used to eliminate self-reactive, pathogenic immune cells while preserving the rest of the immune system.
Autoimmune disease occurs when immune cells 'go rogue' and attack healthy parts of the body, instead of attacking infectious microbes. There are over 100 different autoimmune diseases, which affect 5-10% of the population and are a major cause of chronic disease in our society. Without a cure, individuals afflicted by these diseases face ongoing clinical care based on suppressing the whole immune system. Current clinical practise treats the symptoms of disease rather than the cause because we don’t have a way to identify and eradicate the individual cells of the immune system that have gone rogue.
Our group has developed innovative cellular genomics technology incorporating single cell sequencing and multi-parameter flow cytometry to identify and isolate self-reactive rogue B cells from patients with the autoimmune diseases Sjögren’s syndrome and lupus. This research has allowed us to track the evolution of these disease causing B cells and highlighted possible targets for therapy.
We are currently recruiting enthusiastic students who are interested in using cutting-edge genomic technology to learn about fundamental mechanisms of the immune system and impact treatment strategies and outcomes in patients with autoimmune diseases.
Singh M, Jackson KJL, Wang JJ, Schofield P, Field MA, Koppstein D, Peters TJ, Burnett DL, Rizzetto S, Nevoltris D, Masle-Farquhar E, Faulks ML, Russell A, Gokal D, Hanioka A, Horikawa K, Colella AD, Chataway TK, Blackburn J, Mercer TR, Langley DB, Goodall DM, Jefferis R, Gangadharan Komala M, Kelleher AD, Suan D, Rischmueller M, Christ D, Brink R, Luciani F, Gordon TP, Goodnow CC, Reed JH. Lymphoma driver mutations in the pathogenic evolution of an iconic human autoantibody. Cell, 2020; 180:878-94.
Reed JH, Gorny MK, Li L, JP Buyon and Clancy RM. Ro52 autoantibodies arise from self-reactive progenitors in a mother of a child with neonatal lupus. J Autoimmun, 2017; 79: 99-104.
Reed JH, Jackson J, Christ D, Goodnow CC. Clonal redemption of autoantibodies by somatic hypermutation away from self-reactivity during human immunization. J Exp Med, 2016; 213(7):1255-65.
Sabouri Z, Perotti S, Spierings E, Humburg P, Yabas M, Bergmann H, Horikawa K, Roots C, Lambe S, Young C, Andrews TD, Field M, Enders A*, Reed JH*, Goodnow CC* IgD attenuates the IgM-induced anergy response in transitional and mature B cells. Nat Commun, 2016; 7:103381. *Equal senior authors
Reed JH. and Gordon TP. Ro60-associated RNA takes its toll on disease pathogenesis. Nat Rev Rheumatol, 2016; 12(3): 136-8
Reed JH, Sim S, Wolin SL, Clancy RM and Buyon JP. Ro60 requires Y RNA for cell surface exposure and inflammation associated with cardiac manifestations of neonatal lupus. J Immunol, 2013; 191: 110-116
Reed JH, Jain M, Lee K, Kandimalla ER, Faridi MH, Buyon JP, Gupta V and Clancy RM. Complement Receptor 3 influences Toll-like receptor 7/8 dependent inflammation: Implications for autoimmune diseases characterized by antibody reactivity to ribonucleoproteins. J Biol Chem, 2013; 288: 9077-9083
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