Immunofluorescence testing in the diagnosis of autoimmune blistering diseases: overview of 10-year experience

Arbache, Samia Trigo; Nogueira, Tarsila Gasparotto; Delgado, Lívia; Miyamoto, Denise; Aoki, Valéria

doi:10.1590/abd1806-4841.20143221

Cited by 40 publications

(32 citation statements)

References 16 publications

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“…Previously, complement activation was considered a major cause of blistering, because immunofluorescence studies of skin biopsies from patients with BP have shown that most patients with BP exhibit C3 deposition. Moreover, according to laboratory investigations, the binding of IgG to murine ColXVII triggers complement activation, mast cell degranulation, and neutrophil infiltration, suggesting that the formation of blistering lesions require both IgG and the recruitment and activation of complement (31–35). Recently, another BP pathomechanism has been advocated in which IgG exerts a direct effect on inducing blistering in patients with BP (36, 37).…”

Section: Introductionmentioning

confidence: 99%

“…Evidence supporting these direct effects of BP IgG has been reported. Immunofluorescence studies have revealed that >10% BP cases are positive for BP IgG but negative for C3 deposition (31, 35). Based on the findings from some case reports, IgG staining shows an intercellular pattern in basal cells rather than a linear deposition along the BMZ (38).…”

Section: Introductionmentioning

confidence: 99%

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Bullous Pemphigoid IgG Induces Cell Dysfunction and Enhances the Motility of Epidermal Keratinocytes via Rac1/Proteasome Activation

Tie

Natsuga

et al. 2019

Front. Immunol.

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Bullous pemphigoid (BP) is an autoimmune disease characterized by the formation of blisters, in which autoantibodies mainly target type XVII collagen (ColXVII) expressed in basal keratinocytes. BP IgG is known to induce the internalization of ColXVII from the plasma membrane of keratinocytes through macropinocytosis. However, the cellular dynamics following ColXVII internalization have not been completely elucidated. BP IgG exerts a precise effect on cultured keratinocytes, and the morphological/functional changes in BP IgG-stimulated cells lead to the subepidermal blistering associated with BP pathogenesis. Based on the electron microscopy examination, BP IgG-stimulated cells exhibit alterations in the cell membrane structure and the accumulation of intracellular vesicles. These morphological changes in the BP IgG-stimulated cells are accompanied by dysfunctional mitochondria, increased production of reactive oxygen species, increased motility, and detachment. BP IgG triggers the cascade leading to metabolic impairments and stimulates cell migration in the treated keratinocytes. These cellular alterations are reversed by pharmacological inhibitors of Rac1 or the proteasome pathway, suggesting that Rac1 and proteasome activation are involved in the effects of BP IgG on cultured keratinocytes. Our study highlights the role of keratinocyte kinetics in the direct functions of IgG in patients with BP.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Bullous Pemphigoid IgG Induces Cell Dysfunction and Enhances the Motility of Epidermal Keratinocytes via Rac1/Proteasome Activation

Tie

Natsuga

et al. 2019

Front. Immunol.

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“…In the literature, Arbache et al have reported DIF has a high sensitivity in diagnosing pemphigus vulgaris. 11 The reasons for a negative DIF may be due to the administration of steroids prior to obtaining tissue for biopsy 2,11 or a technical glitch as in this case.…”

Section: Discussionmentioning

confidence: 99%

Juvenile Pemphigus Vulgaris as a Differential Diagnosis for Chronic Generalized Oral Ulceration in an Adolescent: A Case Report and a Review of Literature

Hettiarachchi¹,

Jayasinghe²,

Gunasena³

et al. 2018

International Journal of Experimental Dental Science

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Pemphigus vulgaris (PV) is an autoimmune disorder involving the mucocutaneous tissues. Pathogenesis of this disease causes auto-antibodies against desmogleins in desmosomes which leads to intraepithelial blister formation. It is a rare but potentially life-threatening disease with a prevalence of 1 to 9 per 1 x 10 9 . The disease has an equal sex predilection and commonly occurs in the 5th and 6th decade of life. Clinically, oral lesions are more evident than skin lesions. Diagnosis of the disease is by clinicopathological correlation with the definitive diagnosis requiring immunofluorescent investigations. The mainstay of treatment involves immunosuppression through the use of corticosteroids and other steroid-sparing agents like dapsone, azathioprine, and methotrexate. Presentation of this entity in an adolescent is a rare occurrence, and this may lead to misdiagnosis of the condition. Quality of life of these patients can be improved by controlling the disease through early diagnosis and necessary management. In this article, we report a case of a 15-year-old male patient diagnosed with Juvenile PV (JPV) and discuss the possibility of pemphigusvulgaris as a differential diagnosis for chronic generalized oral ulceration in an adolescent with a brief review of the literature.

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“…In epidermolysis bullosa, immune mapping shows antibodies to the hemidesmosomal antigen and lamina densa protein (e.g., type IV collagen) at the dermo-epidermal junction [ 16 ]. Bullous pemphigoid and epidermolysis bullosa acquisita usually exhibit a linear band of immunoglobulin G deposit along the dermo-epidermal junction [ 17 ]. A U-serrated pattern is typical of epidermolysis bullosa acquisita, whereas a N-serrated pattern is typical of pemphigoid [ 3 ].…”

Section: Discussionmentioning

confidence: 99%

Bullosis Diabeticorum: A Rare Presentation with Immunoglobulin G (IgG) Deposition Related Vasculopathy. Case Report and Focused Review

et al. 2018

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Patient: Male, 42Final Diagnosis: Bullosis diabeticorumSymptoms: Skin rashMedication: —Clinical Procedure: DebridementSpecialty: Metabolic Disorders and DiabeticsObjective:Rare co-existance of disease or pathologyBackground:Bullosis diabeticorum (BD) is a condition characterized by recurrent, spontaneous, and non-inflammatory blistering in patients with poorly controlled diabetes mellitus. While etiopathogenesis remains unclear, roles of neuropathy, vasculopathy and UV light are hypothesized. Most literature reports negative direct and indirect immunofluorescence findings in diabetics with bullous eruptions. Porphyria cutanea tarda, bullous pemphigoid, epidermolysis bullosa, and pseudoporphyria are other differential diagnoses of bullous lesions, and they must be excluded.Case Report:We present a 42-year-old African American male with long standing poorly controlled insulin dependent diabetes mellitus with blisters on his left hand and feet. The blisters were noticed three weeks prior to presentation and, thereafter, rapidly increased in size and spontaneously ruptured. Physical examination revealed a multitude of both roofed and unroofed bullous painless skin lesions. Hematoxylin and eosin (H&E) staining dramatized the dermal-epidermal blistering and re-epithelization process. Direct Immunofluorescence (DIF) was positive for 2 + IgG deposition in the already thickened basement membrane of the capillaries of the superficial vascular plexus. After debridement, his wounds greatly improved with over three months of aggressive wound care.Conclusions:Primary immunologic abnormality likely plays no role in the onset of BD. To date, only one article has reported nonspecific capillary-associated immunoglobulin M and C3. This is the first case of BD with IgG deposition in the superficial capillary basement membrane. Positive findings on DIF suggest vasculopathy. Dermal microangiopathy, secondary to immunologic abnormality, is a possible underlying pathogenesis to bullae formation. Punch biopsy with DIF can be an additional diagnostic modality in the management of such cases.

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Immunofluorescence testing in the diagnosis of autoimmune blistering diseases: overview of 10-year experience

Cited by 40 publications

References 16 publications

Bullous Pemphigoid IgG Induces Cell Dysfunction and Enhances the Motility of Epidermal Keratinocytes via Rac1/Proteasome Activation

Bullous Pemphigoid IgG Induces Cell Dysfunction and Enhances the Motility of Epidermal Keratinocytes via Rac1/Proteasome Activation

Juvenile Pemphigus Vulgaris as a Differential Diagnosis for Chronic Generalized Oral Ulceration in an Adolescent: A Case Report and a Review of Literature

Bullosis Diabeticorum: A Rare Presentation with Immunoglobulin G (IgG) Deposition Related Vasculopathy. Case Report and Focused Review

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