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The term "various soluble and cell-surface antigens recognized by donor B cell receptors" refers to the diverse array of host-derived molecules that act as ligands for B cells originating from a donor, typically in the context of allogeneic hematopoietic stem cell transplantation (HSCT). These antigens are central to the pathogenesis of chronic graft-versus-host disease (cGvHD), where donor B cells escape immune tolerance and mount a response against recipient tissues (Sarantopoulos et al., 2015). Upon binding to these antigens, the donor B-cell receptor (BCR) initiates intracellular signaling cascades, notably involving Bruton's tyrosine kinase (BTK), which leads to B-cell proliferation, differentiation into plasma cells, and the secretion of pathogenic alloantibodies (Miklos et al., 2017). Because these antigens are numerous, heterogeneous, and vary between individual patients, they are not targeted directly by therapeutic agents. Instead, clinical strategies focus on modulating the B cells themselves or inhibiting the signaling pathways activated by these antigens. Common treatments include B-cell depletion using anti-CD20 monoclonal antibodies like rituximab or the inhibition of BCR signaling using small molecules like ibrutinib, which is FDA-approved for cGvHD (Waller, 2017).
Inhibition of B-cell receptor signaling pathways (e.g., BTK inhibition) or depletion of B cells that recognize these antigens.
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