Serum Eosinophil Cationic Protein, Myeloperoxidase, Tryptase, Eotaxin and Th2-Like Cytokines in Dermatitis herpetiformis

Caproni, Marzia; Cardinali, Carla; A, D'agata; Walter, Selvaggi; Fabbri, Paolo

doi:10.1159/000058005

Cited by 12 publications

(8 citation statements)

References 32 publications

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“…Similar behaviour may be found in DH, which is considered to be a Th1/Th2 skin disorder in which neutrophils are thought to be the major effector cells mediating inflammation, with eosinophils playing only an ancillary role [27,28]. In fact, our patients with only mild clinical pictures did not show any systemic activation of coagulation or skin TF expression, although it has been suggested that coagulation activation plays a role in the pathogenesis of DH [29].…”

Section: Discussionsupporting

confidence: 77%

Activation of coagulation in bullous pemphigoid and other eosinophil-related inflammatory skin diseases

Marzano

Tedeschi

Berti

et al. 2011

Clinical and Experimental Immunology

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SummaryBullous pemphigoid (BP) is a skin disease caused by autoantibodies to hemidesmosomal proteins BP180 and BP230, with eosinophils participating in blister formation. Tissue factor (TF), the initiator of coagulation, is embodied within the eosinophil granules and exposed upon activation. We evaluated the coagulation activation in patients with BP (63), chronic urticaria (CU; 20), atopic dermatitis (AD; 14), cutaneous drug reactions (CDRs; six), psoriasis (20), dermatitis herpetiformis (DH; four) and primary cutaneous T cell lymphoma (CTCL; five), and in 40 healthy controls. Prothrombin fragment F1+2 and d-dimer (coagulation markers) were measured by enzyme-linked immunosorbent assay (ELISA) in all plasma samples and BP blister fluid. Skin TF expression was evaluated immunohistochemically in the patients and 20 controls. F1+2 and d-dimer levels were higher in BP plasma than in control plasma (P = 0·0001 for both), and dramatically high in blister fluid; both correlated positively with disease severity, esinophil counts and anti-BP180 antibodies (P = 0·006-0·0001). Plasma F1+2 and d-dimer levels were higher in the CU, AD and CDR patients than in controls (P = 0·0001 for all), but normal in the psoriasis, DH and CTCL patients. Skin TF was expressed in the BP (P = 0·0001), CU (P = 0·0001), AD (P = 0·001) and CDR patients (P = 0·01), but not in the psoriasis, DH or CTCL patients. Co-localization confocal microscopy studies confirmed eosinophils as the source of TF in 10 BP patients. The coagulation cascade is activated in BP and other eosinophilmediated skin disorders, but not in non-eosinophil driven conditions. This hypercoagulability may contribute to inflammation, tissue damage and, possibly, thrombotic risk.

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Section: Discussionsupporting

confidence: 77%

Activation of coagulation in bullous pemphigoid and other eosinophil-related inflammatory skin diseases

Marzano

Tedeschi

Berti

et al. 2011

Clinical and Experimental Immunology

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“…5,19 Although EoE is generally considered a Th2mediated disease 7,26,27 and CD is a Th1-mediated phenomenon, 12 our findings raise the question of whether cases of EoE that resolve with gluten avoidance could be a Th2-mediated manifestation of gluten sensitivity. 28,31,32 This same cytokine profile is well documented in EoE. EoE and DH share certain epidemiologic, histologic, and immunologic features.…”

Section: Discussionmentioning

confidence: 60%

Co-occurrence of eosinophilic esophagitis and potential/probable celiac disease in an adult cohort: a possible association with implications for clinical practice

2015

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We describe an adult cohort with eosinophilic esophagitis (EoE) and evidence of celiac disease (CD), propose a change in diagnostic practice to better characterize these conditions, and hypothesize new directions for research. Pediatric studies postulate association between gluten sensitivity and EoE. However, few publications describe the prevalence, detection, or therapeutic and pathophysiologic implications of such association in adults. Retrospective chart review was done on patients diagnosed with EoE from 2009 to 2010 at University of Utah Hospitals and Clinics. Data included sex, age, presentation, duodenal pathology, tissue transglutaminase immunoglobulin A antibody (TTG) positivity, human leukocyte antigen (HLA) type (when indicated), and gross and microscopic Esophagogastroduodenoscopy (EGD) findings. Duodenal biopsy, TTG results, and HLA type were correlated. Endoscopy was repeated after gluten-free diet. Forty-four of 75 patients were followed in EoE specialty clinic with duodenal biopsy and TTG testing per protocol. Six EoE patients had potential or probable CD. No sex or age differences were noted between those with findings of CD and EoE and those with EoE alone. Six patients with findings of CD and EoE followed gluten-free diet. Five underwent repeat endoscopy. Three had resolution of esophageal eosinophilia. Potential or probable CD was commonly found in adults with EoE. Diagnosis of CD may be challenging due to nonspecific symptoms and insufficient duodenal biopsy and serologic testing. Furthermore, gluten-free diet resolved EoE findings in some patients, suggesting possible shared pathophysiology in some cases of EoE and CD. TTG testing and adequate duodenal biopsy may further direct clinical care for EoE patients, and studies are needed to elucidate mechanisms linking EoE and CD.

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“…Pemphigus and pemphigoid are considered to be prototypic bullous disorders based on their well-characterized immune response-mediated pathogenesis (3)(4)(5). Apart from pemphigus and BP, there is only circumstantial evidence that autoreactive T cells are present and involved in the pathogenesis of the autoimmune bullous disorders epidermolysis bullosa acquisita (6, 7) and dermatitis herpetiformis (8,9). In pemphigus vulgaris (PV) and BP, autoreactive CD4 + T lymphocytes that are presumably crucial in initiating the autoimmune response recognize distinct epitopes of the extracellular portions of Dsg3 and BP180, components of desmosomal and hemidesmosomal adhesion complexes of human skin, respectively.…”

mentioning

confidence: 99%

T cell control in autoimmune bullous skin disorders

Hertl¹

2006

Journal of Clinical Investigation

198

129

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Autoimmune bullous disorders are a group of severe skin diseases characterized clinically by blisters and erosions of skin and/or mucous membranes. A hallmark of these disorders is the presence of IgG and occasionally IgA autoantibodies that target distinct adhesion structures of the epidermis, dermoepidermal basement membrane, and anchoring fibrils of the dermis. This Review focuses on the potential role of autoreactive T cells in the pathogenesis of these disorders. Pemphigus vulgaris (PV) and bullous pemphigoid (BP) are the best-characterized bullous disorders with regard to pathogenesis and T cell involvement. Activation of autoreactive T cells in PV and BP is restricted by distinct HLA class II alleles that are prevalent in individuals with these disorders. Autoreactive T cells are not only present in patients but can also be detected in healthy individuals. Recently, a subset of autoreactive T cells with remarkable regulatory function was identified in healthy individuals and to a much lesser extent in patients with PV, suggesting that the occurrence of autoimmune bullous disorders may be linked to a dysfunction of Tregs.Autoimmune bullous skin disorders are characterized by the presence of autoantibodies that target distinct adhesion molecules of the epidermis and dermoepidermal basement membrane zone, leading to a loss of adhesive function of the target antigen(s) and, clinically, to the appearance of blisters and erosions (1, 2) (Figures 1 and 2). Desmogleins are transmembranous components of desmosomes, adhesion units specialized in conferring epidermal keratinocyte cohesion and linked to intercellular molecules of the desmosomal plaque, which in turn interact with components of the cytoskeleton (Figure 1). In pemphigus, IgG autoantibodies against desmoglein 3 (Dsg3) and Dsg1 lead to loss of desmosomal adhesion of epidermal keratinocytes and intraepidermal blister formation (Figure 2). In the pemphigoids, IgG autoantibodies against components of the dermoepidermal basement membrane such as bullous pemphigoid (BP) antigen 180 (BP180; also referred to as BP antigen 2 and type XVII collagen), BP antigen 230 (BP230; also referred to as BP antigen 1), and laminin 5 interfere with the adhesion of basal epidermal keratinocytes to the dermoepidermal basement membrane zone (Figure 1). BP180 and BP230 are transmembranous and intracellular components, respectively, of hemidesmosomes of basal epidermal keratinocytes, while laminin 5 is a ligand of BP180 located in the lamina lucida of the basement membrane zone (Figure 1). The autoantigen of epidermolysis bullosa, type VII collagen, is the major component of anchoring fibrils that connect the dermoepidermal basement membrane with interstitial collagen bundles of the dermis (Figure 1). The autoantigen of dermatitis herpetiformis, epidermal transglutaminase, is targeted by autoantibodies of the IgA class in the papillary dermis (Figure 2).Based on the specificity of the targeted antigens, several clinically and immune serologically distinct bullous disorders have be...

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Serum Eosinophil Cationic Protein, Myeloperoxidase, Tryptase, Eotaxin and Th2-Like Cytokines in Dermatitis herpetiformis

Cited by 12 publications

References 32 publications

Activation of coagulation in bullous pemphigoid and other eosinophil-related inflammatory skin diseases

Activation of coagulation in bullous pemphigoid and other eosinophil-related inflammatory skin diseases

Co-occurrence of eosinophilic esophagitis and potential/probable celiac disease in an adult cohort: a possible association with implications for clinical practice

T cell control in autoimmune bullous skin disorders

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