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Precision targeting of CD38 in immune thrombocytopenia: Mechanistic foundations and therapeutic implications
Xin Zhou1, Yulu Liu2, Peipei Zhang3
1Department of Hematology, The Second Qilu Hospital of Shandong University, 247 Beiyuan Road, Jinan, 250033, Shandong, China; Department of Hematology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, 250021, China.
Immune thrombocytopenia (ITP) is a multifactorial autoimmune disorder in which antibody-mediated platelet clearance and impaired megakaryopoiesis converge to drive thrombocytopenia and bleeding risk. Guideline-recommended first-line therapies often induce transient responses, yet durable remission is uncommon and many patients remain exposed to relapsing or refractory disease. A central mechanism of persistence is the trafficking of spleen-derived, antigen-specific plasmablasts to the bone marrow, where they differentiate into long-lived plasma cells that sustain antiplatelet autoantibody production. CD38, a multifunctional ectoenzyme and surface receptor expressed on plasma cells, B cells, NK cells, macrophages, and activated T cells, integrates NAD+/Ca2+ signalling with cellular crosstalk within these niches. CD38-directed monoclonal antibodies offer a rational strategy to target this terminal autoantibody reservoir while reshaping effector pathways: they deplete plasmablasts and plasma cells, attenuate Fcγ receptor-mediated phagocytosis, and modulate cytotoxic lymphocyte activity, collectively promoting platelet recovery. This review synthesises CD38 biology in the context of ITP pathogenesis, evaluates the emerging clinical evidence for CD38-targeted interventions, and outlines how biomarker-guided, combination-based strategies might redefine future treatment algorithms.
Immune thrombocytopenia (ITP) is a multifactorial autoimmune disorder in which antibody-mediated platelet clearance and impaired megakaryopoiesis converge to drive thrombocytopenia and bleeding risk. Guideline-recommended first-line therapies often induce transient responses, yet durable remission is uncommon and many patients remain exposed to relapsing or refractory disease. A central mechanism of persistence is the trafficking of spleen-derived, antigen-specific plasmablasts to the bone marrow, where they differentiate into long-lived plasma cells that sustain antiplatelet autoantibody production. CD38, a multifunctional ectoenzyme and surface receptor expressed on plasma cells, B cells, NK cells, macrophages, and activated T cells, integrates NAD+/Ca2+ signalling with cellular crosstalk within these niches. CD38-directed monoclonal antibodies offer a rational strategy to target this terminal autoantibody reservoir while reshaping effector pathways: they deplete plasmablasts and plasma cells, attenuate Fcγ receptor-mediated phagocytosis, and modulate cytotoxic lymphocyte activity, collectively promoting platelet recovery. This review synthesises CD38 biology in the context of ITP pathogenesis, evaluates the emerging clinical evidence for CD38-targeted interventions, and outlines how biomarker-guided, combination-based strategies might redefine future treatment algorithms.
