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1 se pathology in both pemphigus foliaceus and pemphigus vulgaris.
2 tis, melanoma, hidradenitis suppurativa, and pemphigus vulgaris.
3 stleman's disease) nor from 19 patients with pemphigus vulgaris.
4 hology resembling that seen in patients with pemphigus vulgaris.
5 naive adult patients with moderate to severe pemphigus vulgaris.
6 ng on the Pharmaceutical Benefits Scheme for pemphigus vulgaris.
7 mycophenolate mofetil for moderate to severe pemphigus vulgaris.
8 serologic outcomes of rituximab treatment of pemphigus vulgaris.
9 d Drug Administration-approved therapies for pemphigus vulgaris.
10 plete remission at 52 weeks in patients with pemphigus vulgaris.
11 mab as a first-line steroid-sparing agent in pemphigus vulgaris.
12 ic options are warranted in the treatment of pemphigus vulgaris.
13 disease course distinct from pathogenesis of pemphigus vulgaris.
14 lticenter studies for rare diseases, such as pemphigus vulgaris.
15 ents with other blistering disorders such as pemphigus vulgaris.
16 ter solid organ transplantation and to treat pemphigus vulgaris.
17 lin is effective in patients with refractory pemphigus vulgaris.
18 vs) from a patient with active mucocutaneous pemphigus vulgaris.
19 We also show that DSG4 is an autoantigen in pemphigus vulgaris.
22 s Skin Disorder Intensity Score (ABSIS), and Pemphigus Vulgaris Activity Score (PVAS) were validated
23 cal and serologic outcomes for patients with pemphigus vulgaris after rituximab therapy will facilita
24 erapeutic strategy known to be effective for pemphigus vulgaris, an autoimmune condition mediated by
25 but it mediates tissue damage in autoimmune pemphigus vulgaris and "IgG4-related disease." Approxima
28 hundred patients with confirmed diagnoses of pemphigus vulgaris and clinical pemphigus lesions (mean
29 n frozen lesional skin of five patients with pemphigus vulgaris and five patients with pemphigus foli
32 for more targeted therapeutic approaches in pemphigus vulgaris and other autoantibody-driven disorde
38 rtain desmosomal blistering diseases such as pemphigus vulgaris and pemphigus foliaceus have non-cell
39 1 (Dsg1) are relevant in the pathogenesis of pemphigus vulgaris and pemphigus foliaceus, including it
40 oplastic pemphigus, as well as patients with pemphigus vulgaris and pemphigus foliaceus, were studied
43 present a promising therapeutic strategy for pemphigus vulgaris and potentially other autoantibody-me
44 in monoclonal antibodies from a patient with pemphigus vulgaris and show that such antibodies have re
45 desmocollin 3 is a pathogenic autoantigen in pemphigus vulgaris and suggest that pemphigus vulgaris i
46 Sera from patients with bullous pemphigoid, pemphigus vulgaris, and cicatricial pemphigoid-like dise
47 odes with accuracy >97% but only one marker, pemphigus vulgaris antigen (PVA), discriminated with 100
49 ce for the transcriptional regulation of the pemphigus vulgaris antigen gene, potentially critical fo
51 duce an NH2-terminally truncated desmoglein (Pemphigus Vulgaris Antigen or Dsg3) in cells known to ex
53 oliaceus and anti-desmoglein 3 antibodies in pemphigus vulgaris are pathogenic as determined by immun
55 lso be at risk to develop an endemic form of pemphigus vulgaris as reported by our co-investigators f
56 of Dsg3 was thus not only restricted by the pemphigus vulgaris associated DRbeta1*0402 allele, but a
57 lpha5 integrins; and sera from patients with pemphigus vulgaris, bullous pemphigoid (BP), and chronic
58 , including psoriasis, pemphigus foliaceous, pemphigus, vulgaris, bullous pemphigoid, and benign chro
59 and mycophenolate mofetil are used to treat pemphigus vulgaris, but they have not been adequately co
60 gG autoantibodies in pemphigus foliaceus and pemphigus vulgaris cause blisters through loss of desmos
64 in 1 and anti-desmoglein 3 autoantibodies in pemphigus vulgaris had predominant IgG4 subclass specifi
65 It has been postulated that the binding of pemphigus vulgaris IgG (PVIgG) to KCs induces "desmosoma
66 rate that desmocollin 3 is an autoantigen in pemphigus vulgaris, illustrated in a patient with mucosa
67 r formation, because pemphigus foliaceus and pemphigus vulgaris immunoglobulin G caused blisters to t
69 passive transfer of pemphigus foliaceus and pemphigus vulgaris immunoglobulin G these mice blistered
70 we assigned patients with moderate-to-severe pemphigus vulgaris in a 1:1 ratio to receive intravenous
71 th pemphigus foliaceus and six patients with pemphigus vulgaris in active disease and remission were
72 that of patients with the autoimmune disease pemphigus vulgaris, in that the mice develop spontaneous
77 tigen in pemphigus vulgaris and suggest that pemphigus vulgaris is a histological reaction pattern th
82 ain component of the first-line treatment of pemphigus vulgaris is high doses of systemic corticoster
84 phigus foliaceus and fogo selvagem induced a pemphigus vulgaris-like skin disease in mice by passive
86 rated positive DIF findings and consisted of pemphigus vulgaris, mucous membrane pemphigoid, lichen p
89 imilar to those that are highly prevalent in pemphigus vulgaris, namely DRbeta1*0402 and DRbeta1*1401
90 aged 18 years with a confirmed diagnosis of pemphigus (vulgaris or foliaceus) and active disease.
91 testing for IgE levels, and 30 controls with pemphigus vulgaris or pemphigus foliaceus were included
92 nclude diseases like MuSK myasthenia gravis, pemphigus vulgaris or thrombotic thrombocytopenic purpur
93 rative responses of T lymphocytes from eight pemphigus vulgaris patients after incubation with Dsg3 a
95 ntibody blockade of desmoglein 3 function in pemphigus vulgaris patients leads to skin blistering (ac
96 first evidence that T cells from a subset of pemphigus vulgaris patients respond to both Dsg1 and Dsg
99 Five women in their 50s, 60s, or 70s with pemphigus vulgaris (Pemphigus Disease Area Index score,
102 receptor T cells (DSG3-CAART) expressing the pemphigus vulgaris (PV) autoantigen DSG3 fused to CD137-
103 ients with the immunoblistering skin disease pemphigus vulgaris (PV) can induce keratinocyte (KC) dys
104 not mucous membranes, whereas patients with pemphigus vulgaris (PV) develop blisters on mucous membr
108 The development of nonhormonal treatment of pemphigus vulgaris (PV) has been hampered by a lack of c
109 nimal model for studying the pathogenesis of pemphigus vulgaris (PV) has been hampered by the unavail
110 om patients with the blistering skin disease pemphigus vulgaris (PV) IgG is reduced in maturated desm
111 t EGF receptor (EGFR) is activated following pemphigus vulgaris (PV) IgG treatment of primary human k
143 In the human autoimmune blistering disease pemphigus vulgaris (PV) pathogenic antibodies bind the d
145 re responsible for blisters in patients with pemphigus vulgaris (PV) stems from the ability of rDsg1
146 mphigoid (BP), pemphigus foliaceus (PF), and pemphigus vulgaris (PV) to test the hypothesis that the
148 esmoglein 3 (Dsg3) in the autoimmune disease pemphigus vulgaris (PV), as well as B cells responding t
149 In the autoimmune skin-blistering disease pemphigus vulgaris (PV), autoantibodies (IgG) target the
151 in the antibody-mediated autoimmune disease pemphigus vulgaris (PV), autoantigen-based chimeric immu
152 ealth is evidenced by the autoimmune disease pemphigus vulgaris (PV), in which autoantibodies against
153 utoantibody-mediated blistering skin disease pemphigus vulgaris (PV), we applied antibody fractions o
154 Patients with the blistering skin disease pemphigus vulgaris (PV), which is caused by autoantibodi
155 There are two major clinical subsets of pemphigus vulgaris (PV)-mucosal PV (mPV) and mucocutaneo
158 otericin B, 3 mg/kg/d, and a young girl with pemphigus vulgaris responded to treatment with voriconaz
160 1 and anti-desmoglein 3 autoantibodies from pemphigus vulgaris sera and examined the pathogenicity o
161 It has been well documented that a subset of pemphigus vulgaris sera have IgG reactivity to both Dsg1
163 istologically identical to those observed in pemphigus vulgaris, suggesting that desmocollin 3 might
165 goid; 2 cases each of linear IgA disease and pemphigus vulgaris were diagnosed; there was 1 case of b
166 tions of lesional skin from 10 patients with pemphigus vulgaris were negative for HHV8 by in situ hyb
168 us foliaceus and eight patients with mucosal pemphigus vulgaris with active disease inhibited the adh
169 mice mimics autoimmunity to desmoglein 3 in pemphigus vulgaris, with mucosal-dominant blistering in