Journal article
Eosinophils Mediate Tissue Injury in the Autoimmune Skin Disease Bullous Pemphigoid
Journal of investigative dermatology, Vol.138(5), pp.1032-1043
05/2018
DOI: 10.1016/j.jid.2017.11.031
PMID: 29246800
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.
Details
- Title: Subtitle
- Eosinophils Mediate Tissue Injury in the Autoimmune Skin Disease Bullous Pemphigoid
- Creators
- Lan Lin - Department of Dermatology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USABin-Jin Hwang - Department of Dermatology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USADonna A Culton - Department of Dermatology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USANing Li - Department of Dermatology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USASusan Burette - Department of Dermatology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USABeverly H Koller - Department of Genetics, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USAKelly A Messingham - Department of Dermatology, University of Iowa, Iowa City, Iowa, USAJanet A Fairley - Department of Dermatology, University of Iowa, Iowa City, Iowa, USAJames J Lee - Mayo Clinic Arizona, Department of Biochemistry and Molecular Biology, Scottsdale, Arizona, USARussell P Hall - Department of Dermatology, Duke University Medical Center, Durham, North Carolina, USALijia An - School of Life Science and Biotechnology, Dalian University of Technology, Dalian, Liaoning, People’s Republic of ChinaLuis A Diaz - Department of Dermatology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USAZhi Liu - Department of Dermatology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA
- Resource Type
- Journal article
- Publication Details
- Journal of investigative dermatology, Vol.138(5), pp.1032-1043
- Publisher
- Elsevier Inc
- DOI
- 10.1016/j.jid.2017.11.031
- PMID
- 29246800
- ISSN
- 0022-202X
- eISSN
- 1523-1747
- Grant note
- DOI: 10.13039/100000002, name: National Institutes of Health, award: AI07924, AI40768, AR06372, R21AI88628, AR32599, RAR061567A
- Language
- English
- Date published
- 05/2018
- Academic Unit
- Dermatology
- Record Identifier
- 9984025446402771
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