2026-06-14T03:38:18Zhttps://repisalud.isciii.es/rest/oai/request

oai:repisalud.isciii.es:20.500.12105/187322024-02-27T15:10:12Zcom_20.500.12105_15322com_20.500.12105_2051col_20.500.12105_16927col_20.500.12105_16963col_20.500.12105_16982

00925njm 22002777a 4500 dc Arias-de la Rosa, Iván author Escudero-Contreras, Alejandro author Ruiz-Ponce, Miriam author Cuesta-López, Laura author Román-Rodríguez, Cristóbal author Pérez-Sánchez, Carlos author Ruiz-Limón, Patricia author Ruiz, Rocío Guzman- author Leiva-Cepas, Fernando author Alcaide, Juan author Segui, Pedro author Plasencia, Chamaida author Martinez-Feito, Ana author Font, Pilar author Ábalos, María C author Ortega, Rafaela author Malagón, María M author Tinahones, Francisco J author Collantes-Estévez, Eduardo author López-Pedrera, Chary author Barbarroja, Nuria author 2022-08-06 We aimed to evaluate the association between adipose tissue (AT) dysfunction, autoimmunity, and disease activity in rheumatoid arthritis (RA). A cross-sectional study including 150 RA patients and 50 healthy donors and longitudinal study with 122 RA patients treated with anti-tumor necrosis factor (TNF)-α, anti-interleukin 6 receptor (IL6R) or anti-CD20 therapies for 6 months were carried out. In vitro experiments with human AT and adipocyte and macrophage cell lines were performed. A collagen-induced arthritis mouse model was developed. The insulin resistance and the altered adipocytokine profile were associated with disease activity, the presence of anti-citrullinated proteins anti-bodies (ACPAs), and worse response to therapy in RA. AT in the context of arthritis is characterized by an inflammatory state alongside the infiltration of macrophages and B/plasmatic cells, where ACPAs can have a direct impact, inducing inflammation and insulin resistance in macrophages and promoting a defective adipocyte differentiation, partially restored by biologicals. 10.1016/j.isci.2022.104893 2589-0042 iScience http://hdl.handle.net/10668/22278 36046189 http://hdl.handle.net/20.500.12105/18732 Health sciences Immunology Rheumatology Pathogenic mechanisms involving the interplay between adipose tissue and auto-antibodies in rheumatoid arthritis.