2026 American Academy of Neurology Abstract Website

Objective:

To investigate the effect of efgartigimod treatment on immune responses to vaccination.

Background:

Treatment with some immunosuppressive and B-cell–depleting therapies may lead to increased risk of severe infections in patients and may reduce immunogenicity of vaccines. Previous studies have demonstrated that efgartigimod, a human IgG1 antibody Fc fragment that reduces levels of IgG (including pathogenic autoantibodies) through neonatal Fc receptor blockade, does not impair cellular and humoral immune responses to antigenic challenges. Rates and severities of severe infections have been similar between efgartigimod- and placebo-treated participants in placebo-controlled studies and have not increased during long-term open-label studies.

Design/Methods:

Across several clinical studies in healthy volunteers and in participants with generalized myasthenia gravis (gMG), chronic inflammatory demyelinating polyneuropathy (CIDP), immune thrombocytopenia (ITP), and pemphigus vulgaris (PV), intravenous efgartigimod or subcutaneous efgartigimod PH20 was administered in various dosing regimens. Vaccine-specific IgG titers and cellular immunity were assessed at multiple timepoints, including prevaccination, ≥4 weeks postvaccination, and ≤1 week after fourth efgartigimod administration (maximal IgG reduction).

Results:

In participants receiving efgartigimod, antigen–specific IgG titers increased from prevaccination to postvaccination, even during maximal IgG reduction. Additional data demonstrating preservation of cellular immune responses during efgartigimod treatment will be presented.

Conclusions:

Efgartigimod’s unique structure as an Fc fragment selectively reduces IgG antibodies and autoantibodies while preserving the ability to mount antigen-specific responses to immunization. This mechanism avoids both broader impacts on immunity and increased risk of infections observed with some immunosuppressive and B-cell–depleting therapies.