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1 s into draining lymph nodes (LNs) 24 h after epicutaneous administration of FITC in naive mice was si
2 immunization with Alum-adsorbed rBet v 1 and epicutaneous administration of rBet v 1 with PDS in comb
3 Inhibition of Met signaling by single-dose epicutaneous administration of the Met kinase-specific i
5 ll versus wild-type BALB/c mice following an epicutaneous allergen-sensitization/challenge model that
10 enetically engineered mice were subjected to epicutaneous antigen sensitization and the development o
12 and the associated lymphoid tissue following epicutaneous application and intracutaneous injection of
14 les were collected 6, 24, and 48 hours after epicutaneous application of Dermatophagoides farinae hou
16 ation into humans was also accomplished with epicutaneous application of fingolimod resolving histami
18 sebaceous glands of mouse ear skin after an epicutaneous application of OA, the most hBD-2-inducible
19 DCs in the generation of immune responses to epicutaneous application of ovalbumin and during contact
21 zed into three groups: (1) models induced by epicutaneous application of sensitizers; (2) transgenic
22 sensitivity responses induced in mice by the epicutaneous application of the haptens FITC and oxazolo
23 eradicated by a simple vaccination strategy: epicutaneous application of the related orthopoxvirus va
24 described an animal model in which repeated epicutaneous applications of a house dust mite extract a
25 o a physiological skin self-Ag desmoglein-3, epicutaneous applications of desmoglein-3 induced tolera
26 ice exhibited an exaggerated Th2 response to epicutaneous but not to intraperitoneal sensitization wi
27 responsible for protective immunity against epicutaneous Candida infections are incompletely charact
29 d as an increase in ear thickness 24 h after epicutaneous challenge, was significantly enhanced in ma
32 ontrast, IL-4(-/-) mice initially exposed to epicutaneous (e.c.) OVA mounted Th2 responses equivalent
34 Allergic skin inflammation in response to epicutaneous (EC) application of ovalbumin to tape-strip
37 ouse model of allergic dermatitis induced by epicutaneous (EC) sensitization with OVA on tape-strippe
38 reviously unknown pathway by which S. aureus epicutaneous exposure promotes skin inflammation involvi
39 ese findings provide the first evidence that epicutaneous exposure to allergens potently primes for E
41 d protein in human skin biopsy samples after epicutaneous exposure to liquid-phase HDI, although the
59 g-specific CD4 and CD8 T cell responses upon epicutaneous immunization, but could not detect a role i
60 antigen delivery through the unbroken skin (epicutaneous immunization, EPI) has immediate relevance
63 nsitized piglets to evaluate the efficacy of epicutaneous immunotherapy (EPIT) for its treatment.
64 ficacy and mechanism of tolerance induced by epicutaneous immunotherapy (EPIT) in a model of food-ind
65 We sought to evaluate the effect of early epicutaneous immunotherapy (EPIT) on further sensitizati
66 of this study was to compare the efficacy of epicutaneous immunotherapy (EPIT) to sublingual immunoth
70 Recently, the safety and early efficacy of epicutaneous immunotherapy were also demonstrated in pat
71 t, and R848 (resiquimod), a TLR7 agonist, in epicutaneous immunotherapy with Bet v 1, the major birch
72 ical trials, including oral, sublingual, and epicutaneous immunotherapy, immunotherapy combined with
76 CD4 and CD8 T cells after needle injection, epicutaneous infection, or vaginal mucosal herpes simple
78 n immunotherapy have been studied, including epicutaneous, intralymphatic, intranasal, and oral immun
80 d allergies; these involve oral, sublingual, epicutaneous, or subcutaneous administration of small am
81 study, we show that Th2 responses induced by epicutaneous OVA exposure (including lung inflammatory r
82 iased allergic skin inflammation elicited by epicutaneous ovalbumin (OVA) sensitization exhibited lar
85 omly assigned patients (1:1:1:1) received an epicutaneous peanut patch containing 50 mug (n = 53), 10
86 esponse to both contact hypersensitivity and epicutaneous protein immunization, and resulted in a dra
87 We show that exposure to antigen via the epicutaneous route primes for marked eosinophilic inflam
90 female mice with ovalbumin (OVA) followed by epicutaneous sensitization and oral challenge of their o
91 vant-free model of food allergy generated by epicutaneous sensitization and reactions triggered by or
94 ersa TLR4 expression rather protects against epicutaneous sensitization to house dust mite allergen D
96 tested in a murine model of EoE elicited by epicutaneous sensitization with Aspergillus fumigatus pr
98 DC in response to various stimuli, including epicutaneous sensitization with hapten and skin infectio
100 tly described murine model of AD elicited by epicutaneous sensitization with ovalbumin (OVA) (1) and
101 lergic skin inflammation induced by repeated epicutaneous sensitization with ovalbumin (OVA), and cha
105 cretion of Th2 cytokines by splenocytes from epicutaneous sensitized TSLPR(-/-) mice in response to O
106 d skin thickening and collagen deposition in epicutaneous-sensitized skin of DeltadblGATA recipients.
107 Liu et al. (2017) define a pathway by which epicutaneous Staphylococcus aureus promotes skin inflamm
109 ct, and identifies novel mechanisms by which epicutaneous tolerance can suppress food-induced anaphyl
115 ractions with virus-infected cells following epicutaneous vaccinia virus (VV) infection of mice.
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