Bullous Pemphigoid: Interaction of Interleukin 5, Anti-Basement Membrane Zone Antibodies and Eosinophils. A Preliminary Observation

Bhol, Kailash; Kumari, Suman; Ahmed, A. Razzaque

doi:10.1006/cyto.2000.0791

Cited by 38 publications

(37 citation statements)

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“…Engineer et al reported circulating anti-BP230 IgE in all six sera while no BP180-specific IgE autoantibodies were detected in sera and blister fluid of these BP patients. [70] In contrast, other studies revealed IgE anti-BP230 and anti-BP180 antibodies in 67% of 67 sera and 50% of 32 sera, respectively. [100,111] IgE anti-BP230 reactivity was associated with local eosinophil accumulation.…”

Section: Bp230-specific Ige Autoantibodiesmentioning

confidence: 94%

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IgE-mediated mechanisms in bullous pemphigoid and other autoimmune bullous diseases

Beek

Schulze

Zillikens

et al. 2015

Expert Review of Clinical Immunology

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Autoimmune bullous diseases (AIBDs) are characterized by autoantibodies against structural proteins of the dermal-epidermal junction (in pemphigoid diseases) and the epidermal/ epithelial desmosomes (in pemphigus diseases). By far, the most common AIBD is bullous pemphigoid, which is immunopathologically characterized by autoantibodies against BP180 (type XVII collagen) and BP230. IgG and, to a lesser extent, IgA autoantibodies are the major autoantibody isotypes in these disorders. IgE autoantibodies are increasingly reported in particular in bullous pemphigoid. The development of specific and sensitive anti-BP180 IgE ELISA systems, the report of two experimental murine models employing IgE autoantibodies against BP180, and the successful treatment of bullous pemphigoid with the anti-IgE antibody omalizumab have raised interest in the role of IgE autoantibodies and the modulation of their production in AIBDs. Here, the relevance of IgE autoantibodies in the diagnosis, pathophysiology, and treatment decisions of AIBDs, with a focus on bullous pemphigoid, is reviewed. ARTICLE HISTORY

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Section: Bp230-specific Ige Autoantibodiesmentioning

confidence: 94%

“…An inflammatory infiltrate rich of eosinophils is, apart from subepidermal splitting, the key histologic feature of BP [69,70] (Figure 2). In this line, blood eosinophilia has been reported in 50-60% of BP patients.…”

Section: Eosinophiliamentioning

confidence: 99%

IgE-mediated mechanisms in bullous pemphigoid and other autoimmune bullous diseases

Beek

Schulze

Zillikens

et al. 2015

Expert Review of Clinical Immunology

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“…Although BP and GABEB are distinct diseases, i.e., the former is an acquired autoimmune disease and the latter a heritable disorder, a common immunological mechanism would exist for the derm-epidermal detachment between BP and GABEB in our patients. Eosinophil infiltration is one of the characteristic early events in BP (Sams and Gammon 1982) and degranulation of eosinophils that invade into the blister's fluid and release their related cytokines may be a part of immune reactions involved in the derm-epidermal detachment in BP (Engineer et al 2001;Bowszyc-Dmochowska and Dmochowski 2002;Van den Bergh and Giudice 2003). It is also likely that anti-COL17A1 antibodies, such as those against the COL17A1 extracellular domain (Nc16a) (Zillikens et al 1997), play a main role in the pathogenesis of BP because the disease is associated with tissue-bound and circulating IgG-type autoantibodies against the basal membrane zone of the stratified epithelium (Perriard et al 1999;Liu and Diaz 2001).…”

Section: Discussionmentioning

confidence: 99%

Eosinophil infiltration in three patients with generalized atrophic benign epidermolysis bullosa from a Japanese family: molecular genetic and immunohistochemical studies

et al. 2005

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Generalized atrophic benign epidermolysis bullosa (GABEB), a subtype of epidermolysis bullosa (EB), is an autosomal recessive skin disease characterized by derm-epidermal separation leading to skin fragility and atrophy and other associated abnormalities. Although a few reports demonstrated that eosinophils are infiltrating beneath bullas in infants with some types of EB, no such condition in adult GABEB patients has been known. Here we report on three adult patients with GABEB from a Japanese family, whose bullous skin lesions showed massive eosinophil infiltration. One of the three patients showed amyloid deposition at the intestine, kidney, and skin. Linkage analysis revealed that GABEB in the family was linked to COL17A1 with a maximum LOD score of 3.08. Mutation analysis identified in the three patients a homozygous insertional mutation, 209-210insCA, in exon 5 of COL17A1. The expression of mutated COL17A1 was confirmed by semiquantitative RT-PCR, but no signals for truncated COL17A1 protein were detected by the immunohistochemical studies using antibodies against BP180. Furthermore, no autoantibody against the mutant protein was detected by western blot analysis. It is thus less likely that autoantibody and/or a local immune reaction in their skin has a primary role in eosinophil infiltration in these patients.

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“…Our recent study on BP showed that the levels of IL-5 in skin blister fluid are significantly higher than in serum, suggesting local rather than systemic production of IL-5 [5]. Unfortunately, there are no techniques available to precisely measure the levels of IL-5 directly in the inflamed conjunctiva.…”

Section: Discussionmentioning

confidence: 99%

Biology of interleukin-5 in ocular cicatricial pemphigoid

Letko

Bhol

Colón

et al. 2002

Graefe's Arch Clin Exp Ophthalmol

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Bullous Pemphigoid: Interaction of Interleukin 5, Anti-Basement Membrane Zone Antibodies and Eosinophils. A Preliminary Observation

Cited by 38 publications

References 50 publications

IgE-mediated mechanisms in bullous pemphigoid and other autoimmune bullous diseases

IgE-mediated mechanisms in bullous pemphigoid and other autoimmune bullous diseases

Eosinophil infiltration in three patients with generalized atrophic benign epidermolysis bullosa from a Japanese family: molecular genetic and immunohistochemical studies

Biology of interleukin-5 in ocular cicatricial pemphigoid

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