Author: Giacomo Cafaro
Toitou et al. (OP0056) investigated the biology of CD74+ synovial fibroblasts (SF) in rheumatoid arthritis (RA) and found that RA T-cells are able to induce the expression of CD74 on SF which, in turn, increase the expression of activation markers on macrophages, such as CD80, CD40 and CD38, thus contributing to inflammation.
Raimondo et al. (OP0088) investigated the molecular changes of entheseal tissue from psoriatic arthritis patients comparing features before and after treatment with secukinumab. Clinical improvement was associated with a reduced infiltration by multiple IL-17A-expressing immune cells, along with an increased prevalence of CD200+ fibroblasts and ILC2 cells, representing a pro-resolving environment.
Liang (OP0115) performed an extensive evaluation of IgG/IgA binding proteins by immunoprecipitation from systemic sclerosis (SSc) patients and healthy control (HC)-derived sera, identifying among multiple proteins, an increased prevalence of anti-PRMT5 autoantibodies in SSc. They found them to be very specific markers of SSc, compared to other connective tissue diseases, and with potential pathogenic activity in terms of induction of fibrosis and inflammation in mouse models.
Wang et al. (OP0224) performed a multi-omic analysis on RA synovial tissue and identified a subgroup of patients characterised by hypomethylation of TNF and IL-6, and hypermethylation of the FGF module, along with increased TNF/IL-6/CD20 and reduced FGF module gene expression that seem to show high rates of response to TNF-inhibition.
Fava et al. (OP0228) performed a proteomic analysis of urine from lupus nephritis patients, identifying CD163, PRTN3 and IL-16 as biomarkers of function loss at three years with an AUC of 0.96, independent of proteinuria levels.
Xu et al. (OP0054) investigated the crosstalk between B cells and fibroblasts in giant cell arteritis (GCA). They found that B cells are capable of inducing a pro-inflammatory phenotype in fibroblasts, also promoting secretion of IL-6, mostly via soluble factors, thus contributing to disease pathogenesis.
Miranda-Carus et al (POS0247) investigated the presence of circulating Tph (CD4+CXCR5+PD1hi) cells in GCA and found that, compared to HC, GCA patients had a higher prevalence of circulating total Tph and activated (ICOS+) TPh cells. Additionally, a lower basal frequency of such cell subtypes was associated with higher rates of disease relapse following treatment.
ABOUT THE AUTHOR
Giacomo Cafaro
Giacomo is an Assistant Professor of Rheumatology and Consultant Rheumatologist at University of Perugia, Italy. His main research interests are T cell biology in autoimmune diseases, psoriatic arthritis, Sjögren’s syndrome and ultrasound in rheumatology.
Giacomo is a member of the Newsletter Sub-committee.