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J Invest Dermatol. 2018 May;138(5):1032-1043. doi: 10.1016/j.jid.2017.11.031. Epub 2017 Dec 12.

Eosinophils Mediate Tissue Injury in the Autoimmune Skin Disease Bullous Pemphigoid.

Author information

1
Department of Dermatology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA; School of Life Science and Biotechnology, Dalian University of Technology, Dalian, Liaoning, People's Republic of China.
2
Department of Dermatology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
3
Department of Genetics, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
4
Department of Dermatology, University of Iowa, Iowa City, Iowa, USA.
5
Mayo Clinic Arizona, Department of Biochemistry and Molecular Biology, Scottsdale, Arizona, USA.
6
Department of Dermatology, Duke University Medical Center, Durham, North Carolina, USA.
7
School of Life Science and Biotechnology, Dalian University of Technology, Dalian, Liaoning, People's Republic of China.
8
Department of Dermatology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA; Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA; Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA. Electronic address: zhi_liu@med.unc.edu.

Abstract

Eosinophils are typically associated with unique inflammatory settings, including allergic inflammation and helminth infections. However, new information suggests that eosinophils contribute more broadly to inflammatory responses and participate in local immune regulation and the tissue remodeling/repair events linked with a variety of diseases. Eosinophilic infiltration has long been a histologic hallmark of bullous pemphigoid (BP), a subepidermal autoimmune blistering disease characterized by autoantibodies directed against basement membrane protein BP180. However, the exact role of eosinophils in disease pathogenesis remains largely unknown. We show here that eosinophils are necessary for IgE autoantibody-mediated BP blister formation in a humanized IgE receptor mouse model of BP. Disease severity is IgE dose dependent and correlates with the degree of eosinophil infiltration in the skin. Furthermore, IgE autoantibodies fail to induce BP in eosinophil-deficient mice, confirming that eosinophils are required for IgE-mediated tissue injury. Thus, eosinophils provide the cellular link between IgE autoantibodies and skin blistering in this murine model of BP. These findings suggest a role for eosinophils in autoimmune disease and have important implications for the treatment of BP and other antibody-mediated inflammatory and autoimmune diseases.

PMID:
29246800
DOI:
10.1016/j.jid.2017.11.031
[Indexed for MEDLINE]

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