Donor-specific antibody response (DSA response) (DSA response)

Donor-specific B lymphocytes and antibody responses represent the humoral arm of the immune system's reaction against a transplanted organ or tissue (Terasaki, 2003). This process begins when recipient B cells recognize foreign human leukocyte antigens (HLA) on the donor graft, leading to activation, germinal center formation, and differentiation into memory B cells and antibody-secreting plasma cells (Colvin & Smith, 2005). The resulting donor-specific antibodies (DSAs) bind to the graft endothelium, triggering the classical complement cascade and recruiting inflammatory cells, which causes tissue damage known as antibody-mediated rejection (AMR) (Sellarés et al., 2012). This pathway is a major cause of both acute and chronic allograft failure across various organ types, including kidney, heart, and lung transplants (Loupy & Lefaucheur, 2018). Therapeutic strategies targeting this response include B-cell depletion using anti-CD20 agents like Rituximab, plasma cell inhibition with proteasome inhibitors like Bortezomib, and the neutralization of circulating antibodies through intravenous immunoglobulin (Walsh et al., 2011). Monitoring DSAs via solid-phase assays is essential for assessing the risk of rejection and guiding clinical immunosuppressive therapy (Tait et al., 2013).

Other names

Donor-specific antibody (DSA) responseB-cell mediated alloimmunityHumoral alloresponseAntibody-mediated rejection pathwayDonor-specific B-cell activation

Therapeutic strategies involve B-cell depletion via anti-CD20 monoclonal antibodies, proteasome inhibition to induce plasma cell apoptosis, blockade of T-cell costimulation to prevent B-cell help, and inhibition of the terminal complement pathway to prevent tissue damage.