Redefining the Role of Autoantibodies in Myasthenia Gravis & Chronic Inflammatory Demyelinating Polyneuropathy to Improve Therapeutic Positioning & Diagnostic Precision
- Interrogating autoantibodies as central but incompletely defined disease drivers, differentiating therapeutic strategies that lower circulating IgG via FcRn blockade, modulate or deplete upstream B-cells, or remove antibodies through plasma exchange to clarify which modality best addresses underlying immune biology rather than simply reducing antibody burden
- Re-examining “seronegativity” as a potential misclassification challenge and whether so-called seronegative MG and CIDP reflect true absence of pathogenic antibodies or limitations in assay sensitivity and testing paradigms to refine patient stratification and avoid biologically inappropriate therapeutic deployment
- Expanding diagnostic and therapeutic focus toward low-frequency or emerging autoantibody targets to increase diagnostic coverage beyond the current majority subset and enabling precision-guided development across heterogeneous patient populations