Abstract

In this issue of Blood, Tanimura et al describe an interaction between certain human leukocyte antigen (HLA) class II alleles and misfolded β2-glycoprotein I (β2GPI). This complex is expressed on the surface of HLA class II–expressing placental endothelial cells, and it is a target for the autoantibodies against β2GPI seen in patients with antiphospholipid syndrome (APS), providing a mechanistic basis for pregnancy-related morbidity in these patients.1

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