Raphael Sanches Peres
EMBO Research Fellow
I concluded my PhD in Brazil at University of São Paulo studying the immunological mechanisms associated with methotrexate resistance in patients with rheumatoid arthritis. I joined to the Fiona Powie’s group at the Kennedy Institute of Rheumatology in 2017 when I got an EMBO Long-Term Fellowship.
I have interest in translational research that investigates the contribution of regulatory T (Treg) cells in the maintenance of the immunological homeostasis and the events linked to Tregs biology that have impact in the development, establishment and resolution of chronic inflammatory diseases, such as rheumatoid arthritis and inflammatory bowel disease. Furthermore, my interest is to develop therapeutic strategies for inflammatory diseases focused in the manipulation of Tregs cells function and also to determine how this cell population could influence in the efficacy of therapeutic agents available in the clinic, such as methotrexate and TNF inhibitors.
TCR and Inflammatory Signals Tune Human MAIT Cells to Exert Specific Tissue Repair and Effector Functions.
Leng T. et al, (2019), Cell rep, 28, 3077 - 3091.e5
TGFβ1 signaling sustains aryl hydrocarbon receptor (AHR) expression and restrains the pathogenic potential of TH17 cells by an AHR-independent mechanism.
de Lima KA. et al, (2018), Cell death dis, 9
Succinate receptor deficiency attenuates arthritis by reducing dendritic cell traffic and expansion of Th17 cells in the lymph nodes.
Saraiva AL. et al, (2018), Faseb j
Smoking-induced aggravation of experimental arthritis is dependent of aryl hydrocarbon receptor activation in Th17 cells.
Talbot J. et al, (2018), Arthritis res ther, 20
TGF-β signalling defect is linked to low CD39 expression on regulatory T cells and methotrexate resistance in rheumatoid arthritis.
Peres RS. et al, (2018), J autoimmun, 90, 49 - 58