HLA-G and systemic lupus erythematosus: In SLE, however, this intercellular transfer is disrupted or misdirected: CD8+ T cells may receive insufficient HLA-G to suppress autoreactivity; B cells may acquire aberrant HLA-G signals that bypass tolerance checkpoints; and dendritic cells, depleted of surface HLA-G, may become hyperactivated, enhancing antigen presentation and inflammatory cytokine release (Chen and Tsokos, 2021).