TY - JOUR
T1 - B-Cells and BAFF in Primary Antiphospholipid Syndrome, Targets for Therapy?
AU - van den Hoogen, Lucas L.
AU - Bisoendial, Radjesh J.
N1 - Publisher Copyright:
© 2022 by the authors.
PY - 2023/12/20
Y1 - 2023/12/20
N2 - Primary antiphospholipid syndrome (PAPS) is a systemic autoimmune disease characterized by thrombosis, pregnancy morbidity, and the presence of antiphospholipid antibodies (aPL). Anticoagulants form the mainstay of treatment in PAPS. A growing number of studies suggest a previously underappreciated role of the immune system in the pathophysiology of PAPS. Although B-cells are strongly implicated in the pathophysiology of other autoimmune diseases such as systemic lupus erythematosus (SLE), little is known about the role of B-cells in PAPS. Shifts in B-cell subsets including increases in plasmablasts and higher levels of BAFF are present in patients with PAPS. However, while treatment with rituximab and belimumab may ameliorate thrombotic and non-thrombotic manifestations of PAPS, these treatments do not reduce aPL serum levels, suggesting that B-cells contribute to the pathophysiology of APS beyond the production of autoantibodies.
AB - Primary antiphospholipid syndrome (PAPS) is a systemic autoimmune disease characterized by thrombosis, pregnancy morbidity, and the presence of antiphospholipid antibodies (aPL). Anticoagulants form the mainstay of treatment in PAPS. A growing number of studies suggest a previously underappreciated role of the immune system in the pathophysiology of PAPS. Although B-cells are strongly implicated in the pathophysiology of other autoimmune diseases such as systemic lupus erythematosus (SLE), little is known about the role of B-cells in PAPS. Shifts in B-cell subsets including increases in plasmablasts and higher levels of BAFF are present in patients with PAPS. However, while treatment with rituximab and belimumab may ameliorate thrombotic and non-thrombotic manifestations of PAPS, these treatments do not reduce aPL serum levels, suggesting that B-cells contribute to the pathophysiology of APS beyond the production of autoantibodies.
UR - http://www.scopus.com/inward/record.url?scp=85145860801&partnerID=8YFLogxK
U2 - 10.3390/jcm12010018
DO - 10.3390/jcm12010018
M3 - Review article
AN - SCOPUS:85145860801
VL - 12
JO - Journal of Clinical Medicine
JF - Journal of Clinical Medicine
SN - 2077-0383
IS - 1
M1 - 18
ER -