Complement C4d is a degradation product of the complement protein C4, which becomes covalently bound to tissues or cell surfaces following activation of the classical or lectin complement pathways. Because C4d is stable and remains attached at sites of complement activation, it serves as a reliable biomarker of local complement activation. Unlike measuring circulating C4 levels, which fluctuate and may not reflect tissue-level activity, C4d provides a more specific snapshot of immune complex–mediated complement activation in vivo.
In research settings, C4d is widely used to study immune-mediated tissue injury and inflammatory processes. Its deposition can be assessed in experimental models of autoimmune disease, transplant rejection, or infectious pathology to understand mechanisms of complement activation and immune complex–driven tissue damage. C4d detection helps quantify local complement activity, track disease progression, and evaluate the efficacy of complement-targeted therapies in preclinical studies.
In clinical settings, C4d is most notably used in transplantation medicine as a biomarker of antibody-mediated rejection (AMR). Detection of C4d in biopsy samples from transplanted organs (such as kidney or heart) indicates complement activation triggered by donor-specific antibodies, guiding immunosuppressive therapy. Additionally, elevated C4d levels in blood or tissues have been investigated as diagnostic or prognostic markers in autoimmune diseases, such as systemic lupus erythematosus, where immune complex formation drives complement activation and tissue injury.
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