Fcγ Receptors III and IV Mediate Tissue Destruction in a Novel Adult Mouse Model of Bullous Pemphigoid.

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Fcγ Receptors III and IV Mediate Tissue Destruction in a Novel Adult Mouse Model of Bullous Pemphigoid. / Schulze, Franziska S; Beckmann, Tina; Nimmerjahn, Falk; Ishiko, Akira; Collin, Mattias; Köhl, Jörg; Goletz, Stephanie; Zillikens, Detlef; Ludwig, Ralf; Schmidt, Enno.

I: American Journal of Pathology, Vol. 184, Nr. 8, 2014, s. 2185-2196.

Forskningsoutput: TidskriftsbidragArtikel i vetenskaplig tidskrift

Harvard

Schulze, FS, Beckmann, T, Nimmerjahn, F, Ishiko, A, Collin, M, Köhl, J, Goletz, S, Zillikens, D, Ludwig, R & Schmidt, E 2014, 'Fcγ Receptors III and IV Mediate Tissue Destruction in a Novel Adult Mouse Model of Bullous Pemphigoid.', American Journal of Pathology, vol. 184, nr. 8, s. 2185-2196. https://doi.org/10.1016/j.ajpath.2014.05.007

APA

CBE

Schulze FS, Beckmann T, Nimmerjahn F, Ishiko A, Collin M, Köhl J, Goletz S, Zillikens D, Ludwig R, Schmidt E. 2014. Fcγ Receptors III and IV Mediate Tissue Destruction in a Novel Adult Mouse Model of Bullous Pemphigoid. American Journal of Pathology. 184(8):2185-2196. https://doi.org/10.1016/j.ajpath.2014.05.007

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Author

Schulze, Franziska S ; Beckmann, Tina ; Nimmerjahn, Falk ; Ishiko, Akira ; Collin, Mattias ; Köhl, Jörg ; Goletz, Stephanie ; Zillikens, Detlef ; Ludwig, Ralf ; Schmidt, Enno. / Fcγ Receptors III and IV Mediate Tissue Destruction in a Novel Adult Mouse Model of Bullous Pemphigoid. I: American Journal of Pathology. 2014 ; Vol. 184, Nr. 8. s. 2185-2196.

RIS

TY - JOUR

T1 - Fcγ Receptors III and IV Mediate Tissue Destruction in a Novel Adult Mouse Model of Bullous Pemphigoid.

AU - Schulze, Franziska S

AU - Beckmann, Tina

AU - Nimmerjahn, Falk

AU - Ishiko, Akira

AU - Collin, Mattias

AU - Köhl, Jörg

AU - Goletz, Stephanie

AU - Zillikens, Detlef

AU - Ludwig, Ralf

AU - Schmidt, Enno

PY - 2014

Y1 - 2014

N2 - Bullous pemphigoid (BP) and epidermolysis bullosa acquisita are subepidermal autoimmune blistering diseases mediated by autoantibodies against type XVII collagen (Col17) and Col7, respectively. For blister formation, Fc-mediated events, such as infiltration of inflammatory cells in the skin, complement activation, and release of proteases at the dermal-epidermal junction, are essential. Although in the neonatal passive transfer mouse model of BP, tissue destruction is mediated by Fcγ receptors (FcγRs) I and III, the passive transfer model of epidermolysis bullosa acquisita completely depends on FcγRIV. To clarify this discrepancy, we developed a novel experimental model for BP using adult mice. Lesion formation was Fc mediated because γ-chain-deficient mice and mice treated with anti-Col17 IgG, depleted from its sugar moiety at the Fc portion, were resistant to disease induction. By the use of various FcγR-deficient mouse strains, tissue destruction was shown to be mediated by FcγRIV, FcγRIII, and FcγRIIB, whereas FcγRI was not essential. Furthermore, anti-inflammatory mediators in already clinically diseased mice can be explored in the novel BP model, because the pharmacological inhibition of FcγRIV and depletion of granulocytes abolished skin blisters. Herein, we extended our knowledge about the importance of FcγRs in experimental BP and established a novel BP mouse model suitable to study disease development over a longer time period and explore novel treatment strategies in a quasi-therapeutic setting.

AB - Bullous pemphigoid (BP) and epidermolysis bullosa acquisita are subepidermal autoimmune blistering diseases mediated by autoantibodies against type XVII collagen (Col17) and Col7, respectively. For blister formation, Fc-mediated events, such as infiltration of inflammatory cells in the skin, complement activation, and release of proteases at the dermal-epidermal junction, are essential. Although in the neonatal passive transfer mouse model of BP, tissue destruction is mediated by Fcγ receptors (FcγRs) I and III, the passive transfer model of epidermolysis bullosa acquisita completely depends on FcγRIV. To clarify this discrepancy, we developed a novel experimental model for BP using adult mice. Lesion formation was Fc mediated because γ-chain-deficient mice and mice treated with anti-Col17 IgG, depleted from its sugar moiety at the Fc portion, were resistant to disease induction. By the use of various FcγR-deficient mouse strains, tissue destruction was shown to be mediated by FcγRIV, FcγRIII, and FcγRIIB, whereas FcγRI was not essential. Furthermore, anti-inflammatory mediators in already clinically diseased mice can be explored in the novel BP model, because the pharmacological inhibition of FcγRIV and depletion of granulocytes abolished skin blisters. Herein, we extended our knowledge about the importance of FcγRs in experimental BP and established a novel BP mouse model suitable to study disease development over a longer time period and explore novel treatment strategies in a quasi-therapeutic setting.

U2 - 10.1016/j.ajpath.2014.05.007

DO - 10.1016/j.ajpath.2014.05.007

M3 - Article

VL - 184

SP - 2185

EP - 2196

JO - American Journal of Pathology

T2 - American Journal of Pathology

JF - American Journal of Pathology

SN - 1525-2191

IS - 8

ER -