CORRELATION BETWEEN T CELL EXHAUSTION AND PROGRESSION, ACTIVITY AND RESPONSE TO TREATMENT IN PATIENTS WITH RHEUMATOID ARTHRITIS.

ONOFRIO, LUISINA; ZACCA, ESTEFANIA; FERRERO, PAOLA V; ACOSTA, CRISTINA; ALONSO, SERGIO; RAMELLO, MARIA CECILIA; MONTES, CAROLINA L; TOSELLO BOARI, JIMENA; MUSSANO, EDUARDO; ONETTI, LAURA; CADILE, ISAAC; JURADO, RAUL; GRUPPI, ADRIANA; ACOSTA RODRIGUEZ E V

Mar del Plata

Congreso; LXIV Reunión científica anual de la Sociedad Argentina de Inmunología, en conjunto con la reunión anual de SAIC y SAFE.; 2016

Sociedad Argentina de Inmunología, en conjunto con la SAIC y SAFE.

(846) CORRELATION BETWEEN T CELL EXHAUSTIONAND PROGRESSION, ACTIVITY AND RESPONSE TOTREATMENT IN PATIENTS WITH RHEUMATOID ARTHRITIS.Luisina I. Onofrio1, Estefanía R. Zacca1, Paola Ferrero1,Cristina Acosta1, Sergio M. Alonso1, M. Cecilia Ramello2,Carolina Montes2, Jimena Tosello Boari2, Eduardo Mussano1,Laura Onetti1, Isaac Cadile1, M. Victoria Gazzoni1, RaúlJurado1, Adriana Gruppi2, Eva Acosta Rodríguez2.1. Hospital Nacional de Clínicas (HNC), Universidad Nacionalde Córdoba, Córdoba, Argentina. 2. BioquímicaClínica, Facultad Ciencias Químicas. Universidad Nacionalde Córdoba, Córdoba, Argentina.Rheumatoid arthritis (RA) is a progressive inflammatory autoimmunedisease with articular and systemic effects. RA pathophysiologyinvolves B and T cells (Tc) and detrimental interactions ofproinflammatory cytokines. Treatment (Tx) includes antirheumaticdrugs and biologic and synthetic agents. T cell exhaustion (Tex), adysfunctional state characterized by loss of effector functions andexpression of inhibitory receptors (IRs), is harmful during infectionsand cancer. As its role remains unexplored in autoimmunity, weaimed to study Tex during RA and its relationship to disease progressionand activity and response to Tx. Fourteen healthy donors(HD) and 35 RA patients (RApt) (15 untreated and 20 with differentTx) were recruited in the Rheumatology Service (Hospital Nacionalde Clínicas) and evaluated at different times post-Tx. Phenotypeand function of different immune subpopulations from peripheralblood were evaluated by flow cytometry. Although the expressionof the IRs CD160 and BTLA was barely modified by different Tx,there was a significant negative correlation (p<0.05) between theexpression of CD160 on CD4 and CD8 Tc and the disease activityscore (DAS28). Also, the% of CD8 Tc coexpressing the IRsBTLA, CD160, PD1 and TIM3 showed a negative correlation withDAS28 (p <0.02). Moreover, the increase in CD160 expressionbetween months 0 and 3 post-Tx correlated to the response to Txaccording to the EULAR criteria: being high, low and negative inRApt with good, moderate/low and poor responses, respectively.In vitro studies showed that the effector function of activated Tcfrom HD can be inhibited by CD160 and BTLA triggering. Whetherthe inhibitory pathway HVEM-CD160/BTLA is operative in RAptremains to be assessed. Altogether, our findings suggest that Texcorrelates with RA disease activity and response to Tx and couldbe used as biomarker. Accordingly, IR triggering could emerge asa new RA Tx to inhibit exacerbated Tc effector function.