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Autoreactive B cell receptors specific for glycoprotein Ib alpha are immunoglobulin receptors expressed on B lymphocytes that mistakenly recognize platelet glycoprotein Ib alpha as an antigen. This aberrant immune recognition leads to the production of pathogenic anti-GPIbα autoantibodies, a central mechanism in certain autoimmune platelet disorders, most notably immune thrombocytopenia (ITP), resulting in platelet clearance and increased risk of bleeding. Such B cell clones are considered promising therapeutic targets for immune cell–directed therapies, including chimeric autoantibody receptor (CAAR) T cells engineered to selectively eradicate these autoreactive B cells without broadly depleting healthy B cells. Autoantibodies from these B cells not only mediate platelet destruction but also correlate with disease severity and resistance to conventional immunosuppressive treatments.
Elimination of autoreactive B cells by CAAR T cells expressing GP Ibα fragment, selectively killing cells with BCRs specific for GP Ibα General B cell depletion (Rituximab)
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