A Comparison of Oral and Topical Corticosteroids in Patients with Bullous Pemphigoid

Joly, P.; Roujeau, Jean‐Claude; Bénichou, Jacques; Picard, Catherine; Dréno, Brigitte; Delaporte, E.; Vaillant, L.; D’Incan, M.; Plantin, P.; Bédane, C.; Young, Paul R.; Bernard, Philippe

doi:10.1056/nejmoa011592

Cited by 570 publications

(577 citation statements)

References 31 publications

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“…In experimental autoimmune encephalomyelitis, GM-CSF is required to sustain neuroinflammation via myeloid cells infiltrating the CNS (14). Given the rising incidence of autoimmune diseases in general and autoimmune bullous dermatoses specifically (53,54), the so far limited therapeutic options (55,56), and the high morbidity and mortality of the patients (54), there is a clear need for novel treatment strategies. In several autoimmune diseases, such as rheumatoid arthritis, inhibition of cytokines or growth factors has dramatically improved the management of these conditions (57)(58)(59)(60)(61).…”

Section: Discussionmentioning

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: Discussionmentioning

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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“…In pemphigus disease, autoantibodies to desmosomal proteins directly cause blister formation, whereas in pemphigoid disease, blister formation requires the activation of immune mechanisms through the Fc portion of the autoantibodies (1,2). Despite improved therapeutic options, the mortality of patients with pemphigus and pemphigoid remains high (3); this can be attributed, in part, to the extent of immunosuppressive therapy (4). Therefore, and because of the increasing incidence (3), there is a clear and unmet medical need for the development of effective and safe therapies for these patients.…”

mentioning

confidence: 99%

Caspase-1–Independent IL-1 Release Mediates Blister Formation in Autoantibody-Induced Tissue Injury through Modulation of Endothelial Adhesion Molecules

Sadeghi

Lockmann

Hund

et al. 2015

The Journal of Immunology

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Although reports documented aberrant cytokine expression in autoimmune bullous dermatoses (AIBDs), cytokine-targeting therapies have not been established in these disorders. We showed previously that IL-6 treatment protected against tissue destruction in experimental epidermolysis bullosa acquisita (EBA), an AIBD caused by autoantibodies to type VII collagen (COL7). The anti-inflammatory effects of IL-6 were mediated by induction of IL-1ra, and prophylactic IL-1ra administration prevented blistering. In this article, we demonstrate elevated serum concentrations of IL-1β in both mice with experimental EBA induced by injection of anti-COL7 IgG and in EBA patients. Increased IL-1α and IL-1β expression also was observed in the skin of anti-COL7 IgG-injected wild-type mice compared with the significantly less diseased IL-1R–deficient or wild-type mice treated with the IL-1R antagonist anakinra or anti–IL-1β. These findings suggested that IL-1 contributed to recruitment of inflammatory cells into the skin. Accordingly, the expression of ICAM-1 was decreased in IL-1R–deficient and anakinra-treated mice injected with anti-COL7. This effect appeared to be specifically attributable to IL-1 because anakinra blocked the upregulation of different endothelial adhesion molecules on IL-1–stimulated, but not on TNF-α–stimulated, cultured endothelial cells. Interestingly, injection of caspase-1/11–deficient mice with anti-COL7 IgG led to the same extent of skin lesions as in wild-type mice. Collectively, our data suggest that IL-1, independently of caspase-1, contributes to the pathogenesis of EBA. Because anti–IL-1β in a prophylactic setting and anakinra in a quasi-therapeutic setting (i.e., when skin lesions had already developed) improved experimental EBA, IL-1 appears to be a potential therapeutic target for EBA and related AIBDs.

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“…[10] From our study, we particularly emphasize the efficiency of class I corticosteroids in the treatment of PG. We believe that, as in bullous pemphigoid [29] class I topical corticosteroids could be used as firstline to reduce the side effects of corticosteroids while maintaining excellent efficiency.…”

Section: Discussionmentioning

confidence: 99%

Pemphigoid gestationis: A Moroccan study

Chakiri¹,

Salim²,

Inani³

et al. 2017

Our Dermatol Online

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A Comparison of Oral and Topical Corticosteroids in Patients with Bullous Pemphigoid

Abstract: Topical corticosteroid therapy is effective for both moderate and severe bullous pemphigoid and is superior to oral corticosteroid therapy for extensive disease.

Cited by 570 publications

References 31 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

Caspase-1–Independent IL-1 Release Mediates Blister Formation in Autoantibody-Induced Tissue Injury through Modulation of Endothelial Adhesion Molecules

Pemphigoid gestationis: A Moroccan study

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