Mitochondrial Autoantibodies and the Role of Apoptosis in Pemphigus Vulgaris

Dana M Hutchison; Anna-Marie Hosking; Ellen M Hong; Sergei A Grando

doi:10.3390/antib11030055

Mitochondrial Autoantibodies and the Role of Apoptosis in Pemphigus Vulgaris

Antibodies (Basel). 2022 Aug 25;11(3):55. doi: 10.3390/antib11030055.

Authors

Dana M Hutchison^{1

2

3}, Anna-Marie Hosking¹, Ellen M Hong^{2

4}, Sergei A Grando^{1

5

6}

Affiliations

¹ Department of Dermatology, University of California Irvine, Irvine, CA 92697, USA.
² Beckman Laser Institute, University of California Irvine, Irvine, CA 92612, USA.
³ Department of Internal Medicine, Riverside Community Hospital, Riverside, CA 92501, USA.
⁴ Hackensack Meridian School of Medicine, Nutley, NJ 07110, USA.
⁵ Department of Biochemistry, University of California Irvine, Irvine, CA 92697, USA.
⁶ Institute for Immunology, University of California Irvine, Irvine, CA 92697, USA.

Abstract

Pemphigus vulgaris (PV) is an IgG autoantibody-mediated, potentially fatal mucocutaneous disease manifested by progressive non-healing erosions and blisters. Beyond acting to inhibit adhesion molecules, PVIgGs elicit a unique process of programmed cell death and detachment of epidermal keratinocytes termed apoptolysis. Mitochondrial damage by antimitochondrial antibodies (AMA) has proven to be a critical link in this process. AMA act synergistically with other autoantibodies in the pathogenesis of PV. Importantly, absorption of AMA inhibits the ability of PVIgGs to induce blisters. Pharmacologic agents that protect mitochondrial function offer a new targeted approach to treating this severe immunoblistering disease.

Keywords: antimitochondrial autoantibodies; apoptosis; pemphigus vulgaris.

Publication types

Review

Grants and funding

P30 AR075047/AR/NIAMS NIH HHS/United States