Kahn P, Ramanujam M, Bethunaickan R et al.
Feinstein Institute for Medical Research, Manhasset, NY, USA.
Arthritis Rheum 2008;58:2824–34.
Editor’s note: The autoantibodies that cause antiphospholipid syndrome (APS) do not respond to conventional immunosuppression, which suggests that they may be derived from a long-lived B cell subset. The (NZW × BXSB) F
1 mouse is a murine model of spontaneous APS. The male offspring of this cross produce anticardiolipin antibodies (aCL) and anti-ribonucleoprotein antibodies by 12 weeks of age, and subsequently develop immune-mediated thrombo-cytopenia, inflammatory glomerulonephritis, and a thrombotic vasculopathy of the small coronary arteries. The current authors hypothesized that blockade of B cell activating factor (BAFF; a cytokine that is crucial forB cell survival and that interacts with three different receptors on B cells: TACI, BAFF-R, and BCMA) may be used to prevent or treat APS in this mouse model. This hypothesis was based on the fact that BAFF expands the B cell compartment, which leads to increased production of immune complexes, and the idea that blocking the interactions of BAFF and its receptors may therefore prevent disease in both the early and latter stages.