Bullous pemphigoid and herpes gestationis autoantibodies recognize a common non-collagenous site on the BP180 ectodomain

Giudice, George J.; Emery, Daryl J.; Zelickson, Brian D.; Anhalt, Grant J.; Liu, Z.; Díaz, Luis A.

doi:10.1016/0923-1811(93)90940-q

Cited by 170 publications

(240 citation statements)

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“…5). 16,17 Epitope mapping using various fragments of COL17 has shown that sera from most BP patients recognize NC16A. 16 ELISA analysis using recombinant COL17 NC16A demonstrated that 94-96% of BP sera reacts to COL17 NC16A peptides.…”

Section: Major Pathogenic Autoantigen: Type XVII Collagen (Col17)mentioning

confidence: 99%

“…16,17 Epitope mapping using various fragments of COL17 has shown that sera from most BP patients recognize NC16A. 16 ELISA analysis using recombinant COL17 NC16A demonstrated that 94-96% of BP sera reacts to COL17 NC16A peptides. 18,19 In addition, several major antigenic sites have been identified within the N-terminal 45 amino acid stretch of NC16A, while the remaining 28 amino acids of NC16A were shown to have no BP-associated epitopes.…”

Section: Major Pathogenic Autoantigen: Type XVII Collagen (Col17)mentioning

confidence: 99%

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What’s new in bullous pemphigoid

Ujiie

Shibaki

Nishie

et al. 2010

The Journal of Dermatology

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Bullous pemphigoid (BP) is the most common autoimmune blistering disease. BP patients have autoantibodies against type XVII collagen (COL17, also called BP180 or BPAG2), a type II transmembrane protein that spans the lamina lucida and projects into the lamina densa of the epidermal basement membrane. The non-collagenous 16A domain of COL17 is considered to contain pathogenic epitopes of BP. The transfer of immunoglobulin (Ig)G from BP patients fails to cause blisters on mouse skin probably due to differences between humans and mice in the amino acid sequence of NC16A pathogenic epitope of COL17. Passive transfer of rabbit IgG antibodies against the murine homolog of human COL17 NC16A triggers immune reactions to COL17 in mice, including complement activation, mast cell degranulation and neutrophilic infiltration, resulting in dermal-epidermal separation. Recent studies using COL17-humanized mice that express human COL17 but lack murine COL17 were the first to demonstrate the pathogenicity of anti-COL17 human BP IgG autoantibodies in vivo. These new findings provide a greater understanding of BP pathomechanisms and facilitate the development of novel specific and efficient therapeutic strategies for BP.

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Section: Major Pathogenic Autoantigen: Type XVII Collagen (Col17)mentioning

confidence: 99%

Section: Major Pathogenic Autoantigen: Type XVII Collagen (Col17)mentioning

confidence: 99%

What’s new in bullous pemphigoid

Ujiie

Shibaki

Nishie

et al. 2010

The Journal of Dermatology

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“…This hemidesmosomal antigen of type XVII collagen (also known as COL17) consists of a globular intracytoplasmic domain and an extracellular component with 15 collagenous domains [7]. In epitope mapping studies, the non-collagenous 16A (NC16A) extracellular region of BP180 was found to be the major pathogenic epitope in BP [8]. Memory B cells specific to this domain have been identified in BP patients [9].…”

Section: Bullous Pemphigoid (Bp)mentioning

confidence: 99%

Bullous Pemphigoid, Mucous Membrane Pemphigoid and Pemphigus Vulgaris: An Update on Pathobiology

Okon

Werth

2014

Curr Oral Health Rep

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“…The disease, previously known as herpes gestationis, is now classified upon the immunologic and histologic features as a member of the pemphigoid group of diseases, more exactly as a unique manifestation of bullous pemphigoid (BP) [10][11][12]. PG similarly to BP is characterized by subepidermal blister formation and by autoantibodies targeting the hemidesmosomal proteins collagen XVII (0BP180 0 BPAg1) and less commonly also BP230 [12][13][14].…”

Section: Pemphigoid Group Of Diseases In Pregnancymentioning

confidence: 99%

Bullous Dermatoses in Pregnancy

Kárpáti

2012

Curr Derm Rep

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This paper reviews the clinics and therapy of some very rare constellations: autoimmune bullous diseases in pregnancy. In this context of the immunology of healthy pregnancy, the term of fetal-maternal tolerance and the consequences of the lost or damaged tolerance during early or late pregnancy will be briefly introduced. We will discuss the course of autoimmune blistering diseases during gravidity, their diagnosis, including differential from other gestational dermatoses and the possible fetal outcome. As the most common of the pregnancy-induced autoimmune blistering diseases, pemphigoid gestationis will be detailed, together with the significant development on fetal-maternal immunology and disease pathology. Management of patients with pemphigus and pemphigoid group of diseases as well as therapy, diet, and follow-up suggested for gravidas with dermatitis herpetiformis will be summarized. The current status and pregnancy safety categories of immunosuppressive and adjuvant treatment modalities will be highlighted.

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Bullous pemphigoid and herpes gestationis autoantibodies recognize a common non-collagenous site on the BP180 ectodomain

Cited by 170 publications

References 0 publications

What’s new in bullous pemphigoid

What’s new in bullous pemphigoid

Bullous Pemphigoid, Mucous Membrane Pemphigoid and Pemphigus Vulgaris: An Update on Pathobiology

Bullous Dermatoses in Pregnancy

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