PMID- 25043618
OWN - NLM
STAT- MEDLINE
DCOM- 20150330
LR  - 20231213
IS  - 1525-2191 (Electronic)
IS  - 0002-9440 (Linking)
VI  - 184
IP  - 8
DP  - 2014 Aug
TI  - Fcgamma receptors III and IV mediate tissue destruction in a novel adult mouse model 
      of bullous pemphigoid.
PG  - 2185-96
LID - S0002-9440(14)00281-8 [pii]
LID - 10.1016/j.ajpath.2014.05.007 [doi]
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 Fcgamma receptors (FcgammaRs) I and III, the passive transfer 
      model of epidermolysis bullosa acquisita completely depends on FcgammaRIV. To clarify 
      this discrepancy, we developed a novel experimental model for BP using adult 
      mice. Lesion formation was Fc mediated because gamma-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 FcgammaR-deficient mouse 
      strains, tissue destruction was shown to be mediated by FcgammaRIV, FcgammaRIII, and 
      FcgammaRIIB, whereas FcgammaRI 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 FcgammaRIV and depletion of 
      granulocytes abolished skin blisters. Herein, we extended our knowledge about the 
      importance of FcgammaRs 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.
CI  - Copyright (c) 2014 American Society for Investigative Pathology. Published by 
      Elsevier Inc. All rights reserved.
FAU - Schulze, Franziska S
AU  - Schulze FS
AD  - Department of Dermatology, University of Lubeck, Lubeck, Germany.
FAU - Beckmann, Tina
AU  - Beckmann T
AD  - Department of Dermatology, University of Lubeck, Lubeck, Germany.
FAU - Nimmerjahn, Falk
AU  - Nimmerjahn F
AD  - Department of Biology, University of Erlangen-Nuremberg, Erlangen, Germany.
FAU - Ishiko, Akira
AU  - Ishiko A
AD  - Department of Dermatology, Toho University School of Medicine, Tokyo, Japan.
FAU - Collin, Mattias
AU  - Collin M
AD  - Division of Infection Medicine, Department of Clinical Science, Lund University, 
      Lund, Sweden.
FAU - Kohl, Jorg
AU  - Kohl J
AD  - Institute for Systemic Inflammation Research, University of Lubeck, Lubeck, 
      Germany.
FAU - Goletz, Stephanie
AU  - Goletz S
AD  - Department of Dermatology, University of Lubeck, Lubeck, Germany.
FAU - Zillikens, Detlef
AU  - Zillikens D
AD  - Department of Dermatology, University of Lubeck, Lubeck, Germany.
FAU - Ludwig, Ralf
AU  - Ludwig R
AD  - Department of Dermatology, University of Lubeck, Lubeck, Germany.
FAU - Schmidt, Enno
AU  - Schmidt E
AD  - Department of Dermatology, University of Lubeck, Lubeck, Germany. Electronic 
      address: enno.schmidt@uksh.de.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Am J Pathol
JT  - The American journal of pathology
JID - 0370502
RN  - 0 (Autoantibodies)
RN  - 0 (Autoantigens)
RN  - 0 (Collagen Type VII)
RN  - 0 (Fcgr3 protein, mouse)
RN  - 0 (Fcgr4 protein, mouse)
RN  - 0 (Non-Fibrillar Collagens)
RN  - 0 (Receptors, IgG)
SB  - IM
MH  - Animals
MH  - Autoantibodies/immunology
MH  - Autoantigens/immunology
MH  - Collagen Type VII/*immunology
MH  - *Disease Models, Animal
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Microscopy, Fluorescence
MH  - Non-Fibrillar Collagens/immunology
MH  - Pemphigoid, Bullous/*immunology/pathology
MH  - Receptors, IgG/*immunology
MH  - Collagen Type XVII
EDAT- 2014/07/22 06:00
MHDA- 2015/03/31 06:00
CRDT- 2014/07/22 06:00
PHST- 2014/02/20 00:00 [received]
PHST- 2014/04/11 00:00 [revised]
PHST- 2014/05/13 00:00 [accepted]
PHST- 2014/07/22 06:00 [entrez]
PHST- 2014/07/22 06:00 [pubmed]
PHST- 2015/03/31 06:00 [medline]
AID - S0002-9440(14)00281-8 [pii]
AID - 10.1016/j.ajpath.2014.05.007 [doi]
PST - ppublish
SO  - Am J Pathol. 2014 Aug;184(8):2185-96. doi: 10.1016/j.ajpath.2014.05.007.