May is CIDP Awareness Month. See how to make progress for your patients here

IgG autoantibodies play a role
in CIDP1,2

The exact pathophysiology of CIDP is complex and not completely understood, but our knowledge of its mechanisms is expanding.1,3

Evidence suggests that IgG autoantibodies may be key to our understanding.1,2

CIDP=chronic inflammatory demyelinating polyneuropathy; IgG=immunoglobulin G.

Discover how IgG autoantibodies can trigger damage in CIDP

CIDP=chronic inflammatory demyelinating polyneuropathy;
IgG=immunoglobulin G.

The role of IgG autoantibodies in CIDP

In patients with CIDP, the binding activity of autoantibodies, including IgG autoantibodies, to the myelin sheath may result in demyelination, subsequent nerve damage, and symptom expression.1,3,4

Infiltration of IgG autoantibodies

Activated T cells trigger inflammatory mediators (cytokines and chemokines) to break the blood-nerve barrier, facilitating the passage of autoantibodies, including IgG autoantibodies.1,2,4

Inflirtation of IgG
Depiction of the two ways that IgG autoantibodies have been shown to contribute to disease progress in CIDP.

1. Activated T cell
2. Cytokines/chemokines
3. Plasma cell
4. IgG autoantibodies

5. Blood-nerve barrier

Demyelination due to IgG autoantibodies

IgG autoantibodies bind to the myelin sheath, where they either recruit macrophages directly or activate the complement pathway, which may result in myelin damage.1-4

Inflirtation of IgG
Depiction of IgG autoantibodies crossing the blood-nerve barrier, along with other inflammatory mediators.

1. IgG autoantibodies
2. Macrophage
3. Fc receptor
4. Myelin sheath

5. Complement proteins

Demyelination can contribute to axonal damage in CIDP and increase the potential for chronic disability.5-7

The GBS|CIDP Foundation estimates

30%

of patients with CIDP progress to
wheelchair dependence if not treated8

The GBS|CIDP Foundation estimates

30%

of patients with CIDP progress to wheelchair dependence if not treated8

CIDP=chronic inflammatory demyelinating polyneuropathy; Fc=fragment, crystallized; GBS=Guillain-Barré syndrome; IgG=immunoglobulin G.

FcRn extends circulation of IgG antibodies, including autoantibodies

FcRn perpetuates the circulation of IgG antibodies, including the autoantibodies that may play a role in disease activity.5-7,9,10 

FcRn perpetuates demyelination image
VYV-CIDP-FcRn-Recycling-mobile

1. IgG antibody
2. Endosome
3. FcRn
4. Lysosome

Understanding how FcRn recycles IgG, including autoantibodies, opens new opportunities for intervention.9,10

FcRn=neonatal Fc receptor; IgG=immunoglobulin G.

You’ve explored the role FcRn plays in CIDP. Now learn about what
happens when it becomes a therapeutic target

CIDP=chronic inflammatory demyelinating polyneuropathy; FcRn=neonatal Fc receptor; MOA=mechanism of action.

argenx is committed to the discovery of innovative solutions to improve the lives of patients with CIDP

References: 1. Mathey EK et al. J Neurol Neurosurg Psychiatry. 2015;86(9):973-985. doi:10.1136/jnnp-2014-309697 2. Querol LA et al. Neurotherapeutics. 2022;19(3):864-873. doi:10.1007/s13311-022-01221-y 3. Dziadkowiak E et al. Int J Mol Sci. 2022;23:2-13. doi:10.3390/ijms23010179 4. Koike H et al. Neurol Ther. 2020;9:213-227. doi:10.1007/s40120-020-00190-8 5. Ricciardi D et al. Brain Sci. 2022;12(11):1510. doi:10.3390/brainsci12111510 6. Al-Zuhairy A et al. Clin Neurophysiol. 2021;132(4):1000-1007. doi:10.1016/j.clinph.2020.12.017 7. Al-Zuhairy A et al. Muscle Nerve. 2022;66(6):715-722. doi:10.1002/mus.27722 8. GBS CIDP Organisation Europe. CIDP. Accessed January 9, 2026. https://eu.gbs-cidp.org/about/cidp/ 9. Ulrichts P et al. J Clin Invest. 2018;128(10):4372-4386. doi:10.1172/JCI97911 10. Wolfe GI et al. J Neurol Sci. 2021;430:118074. doi:10.1016/j.jns.2021.118074