Pathogenicity of IgG subclass autoantibodies to type VII collagen: Induction of dermal–epidermal separation

Recke, Andreas; Sitaru, Cassian; Vidarsson, Gestur; Evensen, Mirja; Chiriac, Mircea T.; Ludwig, Ralf J.; Zillikens, Detlef

doi:10.1016/j.jaut.2009.11.003

Cited by 50 publications

(61 citation statements)

References 59 publications

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“…In brief, human PMNs were isolated using Polymorphprep (Axis-Shield, Heidelberg, Germany) following the protocol provided by the manufacturer. Isolated PMNs were incubated on a 96-well plate (Greiner Bio-One, Frickenhausen, Germany) coated with IC formed by monoclonal anti-COL7 Abs and recombinant fragments located within the human NC1 domain of COL7 (38). ROS release with GM-CSF at different concentrations was analyzed using luminol (Sigma-Aldrich Biochemie, Hamburg, Germany).…”

Section: Measurement Of Reactive Oxygen Species and Gm-csf Release Frmentioning

confidence: 99%

GM-CSF Modulates Autoantibody Production and Skin Blistering in Experimental Epidermolysis Bullosa Acquisita

Samavedam

Iwata

Müller

et al. 2014

The Journal of Immunology

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GM-CSF activates hematopoietic cells and recruits neutrophils and macrophages to sites of inflammation. Inhibition of GM-CSF attenuates disease activity in models of chronic inflammatory disease. Effects of GM-CSF blockade were linked to modulation of the effector phase, whereas effects on early pathogenic events, for example, Ab production, have not been identified. To evaluate yet uncharacterized effects of GM-CSF on early pathogenic events in chronic inflammation, we employed immunization-induced epidermolysis bullosa acquisita (EBA), an autoimmune bullous disease caused by autoantibodies to type VII collagen. Compared to wild-type mice, upon immunization, GM-CSF−/− mice produced lower serum autoantibody titers, which were associated with reduced neutrophil numbers in draining lymph nodes. The same effect was observed in neutrophil-depleted wild-type mice. Neutrophil depletion in GM-CSF−/− mice led to a stronger inhibition, indicating that GM-CSF and neutrophils have additive functions. To characterize the contribution of GM-CSF specifically in the effector phase of EBA, disease was induced by transfer of anti–type VII collagen IgG into mice. We observed an increased GM-CSF expression, and GM-CSF blockade reduced skin blistering. Additionally, GM-CSF enhanced reactive oxygen species release and neutrophil migration in vitro. In immunization-induced murine EBA, treatment with anti–GM-CSF had a beneficial effect on established disease. We demonstrate that GM-CSF modulates both autoantibody production and skin blistering in a prototypical organ-specific autoimmune disease.

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Section: Measurement Of Reactive Oxygen Species and Gm-csf Release Frmentioning

confidence: 99%

GM-CSF Modulates Autoantibody Production and Skin Blistering in Experimental Epidermolysis Bullosa Acquisita

Samavedam

Iwata

Müller

et al. 2014

The Journal of Immunology

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“…responses to vaccination, autoantibodies (9)(10)(11)(12), alloimmunization to transfusion and transplantation antigens (13,14), and maternal alloantibodies against fetal and paternal antigens (15)(16)(17). In addition, IgG subclass deficiency is among the more common immunodeficiencies in pediatric populations, resulting in increased rates of particular infections (18,19).…”

Section: Introductionmentioning

confidence: 99%

Errors in data interpretation from genetic variation of human analytes

Howie¹,

Delaney²,

Wang³

et al. 2017

JCI Insight

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“…IgG isotype level analyses have been done to define any predominance of T H 1-versus T H 2-type cell-mediated immune responses that might influence the pathogenesis of various diseases (Krieger et al, 2013;Recke et al, 2010;Xu et al, 2006). In addition, IgG isotypes (against specific autoantigens) have been investigated for any potential contribution to the induction or relapse of certain autoimmune diseases (Bijl et al, 2002;Gao et al, 2006;Kosuda et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

Aberrant IgG isotype generation in mice with abnormal behaviors

Kim

et al. 2015

Journal of Immunotoxicology

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BTBR T+tf/J (BTBR) mice were recently cited as a suitable animal model for the study of autism because of their behavioral characteristics and immunological changes similar to those reported from autistic subjects. The BTBR mouse was reported to have significantly higher levels of serum IgG, brain IgG deposits and anti-brain IgG than highly social C57BL/6 mice, suggesting involvement of aberrant immune responses in the occurrence of autism. Upregulation of IgG production was investigated here, with a focus on the pattern of IgG isotype distribution compared with that in FVB/NJ (FVB) mice, another highly social control strain. The results indicated that levels of serum IgG 1 , IgG 2b and IgG 3 in post-natal day 21 BTBR mice was significantly higher than FVB mice, regardless of sex, resulting in higher IgG 1 :IgG 2a ratios in BTBR mice than in FVB mice (statistical significance in males). A similar outcome regarding the IgG 1 :IgG 2a ratio was observed in culture supernatants of bone marrow cells from these hosts. A presence of brain-reactive IgG in the sera of BTBR was higher than in FVB mice; levels of brainreactive IgG against whole brain homogenates were higher in BTBR than in FVB mice, with significant differences seen in the striatum and substantia nigra regions. Levels of IgG 1 deposited in the cerebellum, cortex, hippocampus or striatum of both BTBR male and female mice were significantly higher than in FVB counterparts. Overall, these results suggest that alterations in IgG isotype production or deposition in the brain could be implicated in the aberrant immune reactivities of BTBR mice.

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Pathogenicity of IgG subclass autoantibodies to type VII collagen: Induction of dermal–epidermal separation

Cited by 50 publications

References 59 publications

GM-CSF Modulates Autoantibody Production and Skin Blistering in Experimental Epidermolysis Bullosa Acquisita

GM-CSF Modulates Autoantibody Production and Skin Blistering in Experimental Epidermolysis Bullosa Acquisita

Errors in data interpretation from genetic variation of human analytes

Aberrant IgG isotype generation in mice with abnormal behaviors

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