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1 tis, melanoma, hidradenitis suppurativa, and pemphigus vulgaris.
2 stleman's disease) nor from 19 patients with pemphigus vulgaris.
3 disease course distinct from pathogenesis of pemphigus vulgaris.
4 lticenter studies for rare diseases, such as pemphigus vulgaris.
5 ents with other blistering disorders such as pemphigus vulgaris.
6 ter solid organ transplantation and to treat pemphigus vulgaris.
7 lin is effective in patients with refractory pemphigus vulgaris.
8 vs) from a patient with active mucocutaneous pemphigus vulgaris.
9 We also show that DSG4 is an autoantigen in pemphigus vulgaris.
10 ic options are warranted in the treatment of pemphigus vulgaris.
13 s Skin Disorder Intensity Score (ABSIS), and Pemphigus Vulgaris Activity Score (PVAS) were validated
14 erapeutic strategy known to be effective for pemphigus vulgaris, an autoimmune condition mediated by
15 but it mediates tissue damage in autoimmune pemphigus vulgaris and "IgG4-related disease." Approxima
17 hundred patients with confirmed diagnoses of pemphigus vulgaris and clinical pemphigus lesions (mean
18 n frozen lesional skin of five patients with pemphigus vulgaris and five patients with pemphigus foli
25 rtain desmosomal blistering diseases such as pemphigus vulgaris and pemphigus foliaceus have non-cell
26 1 (Dsg1) are relevant in the pathogenesis of pemphigus vulgaris and pemphigus foliaceus, including it
27 oplastic pemphigus, as well as patients with pemphigus vulgaris and pemphigus foliaceus, were studied
30 in monoclonal antibodies from a patient with pemphigus vulgaris and show that such antibodies have re
31 desmocollin 3 is a pathogenic autoantigen in pemphigus vulgaris and suggest that pemphigus vulgaris i
32 Sera from patients with bullous pemphigoid, pemphigus vulgaris, and cicatricial pemphigoid-like dise
33 odes with accuracy >97% but only one marker, pemphigus vulgaris antigen (PVA), discriminated with 100
35 ce for the transcriptional regulation of the pemphigus vulgaris antigen gene, potentially critical fo
37 duce an NH2-terminally truncated desmoglein (Pemphigus Vulgaris Antigen or Dsg3) in cells known to ex
39 oliaceus and anti-desmoglein 3 antibodies in pemphigus vulgaris are pathogenic as determined by immun
41 lso be at risk to develop an endemic form of pemphigus vulgaris as reported by our co-investigators f
42 of Dsg3 was thus not only restricted by the pemphigus vulgaris associated DRbeta1*0402 allele, but a
43 lpha5 integrins; and sera from patients with pemphigus vulgaris, bullous pemphigoid (BP), and chronic
44 , including psoriasis, pemphigus foliaceous, pemphigus, vulgaris, bullous pemphigoid, and benign chro
48 in 1 and anti-desmoglein 3 autoantibodies in pemphigus vulgaris had predominant IgG4 subclass specifi
49 It has been postulated that the binding of pemphigus vulgaris IgG (PVIgG) to KCs induces "desmosoma
50 rate that desmocollin 3 is an autoantigen in pemphigus vulgaris, illustrated in a patient with mucosa
51 r formation, because pemphigus foliaceus and pemphigus vulgaris immunoglobulin G caused blisters to t
53 passive transfer of pemphigus foliaceus and pemphigus vulgaris immunoglobulin G these mice blistered
54 that of patients with the autoimmune disease pemphigus vulgaris, in that the mice develop spontaneous
58 tigen in pemphigus vulgaris and suggest that pemphigus vulgaris is a histological reaction pattern th
62 ain component of the first-line treatment of pemphigus vulgaris is high doses of systemic corticoster
64 phigus foliaceus and fogo selvagem induced a pemphigus vulgaris-like skin disease in mice by passive
65 rated positive DIF findings and consisted of pemphigus vulgaris, mucous membrane pemphigoid, lichen p
67 imilar to those that are highly prevalent in pemphigus vulgaris, namely DRbeta1*0402 and DRbeta1*1401
68 testing for IgE levels, and 30 controls with pemphigus vulgaris or pemphigus foliaceus were included
69 rative responses of T lymphocytes from eight pemphigus vulgaris patients after incubation with Dsg3 a
71 ntibody blockade of desmoglein 3 function in pemphigus vulgaris patients leads to skin blistering (ac
72 first evidence that T cells from a subset of pemphigus vulgaris patients respond to both Dsg1 and Dsg
75 Five women in their 50s, 60s, or 70s with pemphigus vulgaris (Pemphigus Disease Area Index score,
77 ients with the immunoblistering skin disease pemphigus vulgaris (PV) can induce keratinocyte (KC) dys
78 not mucous membranes, whereas patients with pemphigus vulgaris (PV) develop blisters on mucous membr
81 The development of nonhormonal treatment of pemphigus vulgaris (PV) has been hampered by a lack of c
82 nimal model for studying the pathogenesis of pemphigus vulgaris (PV) has been hampered by the unavail
83 om patients with the blistering skin disease pemphigus vulgaris (PV) IgG is reduced in maturated desm
84 t EGF receptor (EGFR) is activated following pemphigus vulgaris (PV) IgG treatment of primary human k
111 In the human autoimmune blistering disease pemphigus vulgaris (PV) pathogenic antibodies bind the d
113 re responsible for blisters in patients with pemphigus vulgaris (PV) stems from the ability of rDsg1
114 mphigoid (BP), pemphigus foliaceus (PF), and pemphigus vulgaris (PV) to test the hypothesis that the
116 esmoglein 3 (Dsg3) in the autoimmune disease pemphigus vulgaris (PV), as well as B cells responding t
117 In the autoimmune skin-blistering disease pemphigus vulgaris (PV), autoantibodies (IgG) target the
119 in the antibody-mediated autoimmune disease pemphigus vulgaris (PV), autoantigen-based chimeric immu
120 ealth is evidenced by the autoimmune disease pemphigus vulgaris (PV), in which autoantibodies against
121 utoantibody-mediated blistering skin disease pemphigus vulgaris (PV), we applied antibody fractions o
122 There are two major clinical subsets of pemphigus vulgaris (PV)-mucosal PV (mPV) and mucocutaneo
124 otericin B, 3 mg/kg/d, and a young girl with pemphigus vulgaris responded to treatment with voriconaz
126 1 and anti-desmoglein 3 autoantibodies from pemphigus vulgaris sera and examined the pathogenicity o
127 It has been well documented that a subset of pemphigus vulgaris sera have IgG reactivity to both Dsg1
129 istologically identical to those observed in pemphigus vulgaris, suggesting that desmocollin 3 might
131 goid; 2 cases each of linear IgA disease and pemphigus vulgaris were diagnosed; there was 1 case of b
132 tions of lesional skin from 10 patients with pemphigus vulgaris were negative for HHV8 by in situ hyb
133 mice mimics autoimmunity to desmoglein 3 in pemphigus vulgaris, with mucosal-dominant blistering in
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