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1 ape-stripping test and in a disease model of contact dermatitis.
2 shiols and related phenols, which can induce contact dermatitis.
3  the development of T-cell-mediated allergic contact dermatitis.
4  are antigenic determinants in patients with contact dermatitis.
5  skin of patients with psoriasis or allergic contact dermatitis.
6  CD8+ T cells from individuals with allergic contact dermatitis.
7 ration of the phorbol ester-induced irritant contact dermatitis.
8 ermatitis and oxazolone, a model of allergic contact dermatitis.
9 lize to immunologically nonspecific forms of contact dermatitis.
10 is, fixed drug eruption, atopic and allergic contact dermatitis.
11 ed utilizing models of irritant and allergic contact dermatitis.
12  sulfate is a well-known inducer of irritant contact dermatitis.
13 nduced skin cancers or allergic and irritant contact dermatitis.
14 g psoriasis, atopic dermatitis, and allergic contact dermatitis.
15 ional skin disease are irritant and allergic contact dermatitis.
16 ns commonly trigger T cell-mediated allergic contact dermatitis.
17 gic contact dermatitis (ACD) and/or irritant contact dermatitis.
18 n immune cells in mouse models of atopic and contact dermatitis.
19 eases such as atopic dermatitis and allergic contact dermatitis.
20 cessful diagnosis and management of allergic contact dermatitis.
21  preservatives is a global cause of allergic contact dermatitis.
22 n psoriasis, atopic dermatitis, and allergic contact dermatitis.
23 new therapeutic approaches to treat allergic contact dermatitis.
24 ng the diagnosis of allergic versus irritant contact dermatitis.
25 at occur within the skin during each type of contact dermatitis.
26 tion through MRGPRB2 drives itch in allergic contact dermatitis.
27 y effect of these NPs in a model of allergic contact dermatitis.
28 tial therapeutic avenue in treating allergic contact dermatitis.
29 presents select aspects of AD, psoriasis, or contact dermatitis.
30 ibitor, ARN077, in a mouse model of allergic contact dermatitis.
31 acterize the role of MCs in chronic allergic contact dermatitis.
32 of murine skin serves as a model of allergic contact dermatitis.
33 bly influence the course of chronic allergic contact dermatitis.
34 igand 1 (CXCL1) in a mouse model of irritant contact dermatitis.
35 the generation of skin TRM cells in allergic contact dermatitis.
36 e risk of contact sensitization and allergic contact dermatitis.
37 rs they are one of the most common causes of contact dermatitis.
38 gical processes like irritative and allergic contact dermatitis.
39 metics, and they are known to cause allergic contact dermatitis.
40 xperimental animal studies to evoke allergic contact dermatitis.
41 atory responses and pruritus associated with contact dermatitis.
42 2.53)], alopecia areata [3.47 (3.24, 3.71)], contact dermatitis [1.92 (1.88, 1.96)], psoriasis [2.62
43 rgic conjunctivitis (25.0%, 8.6%: p = 0.02), contact dermatitis (4.2%, 4.4%: p = 1.0), and asthma (4.
44 ypersensitivity, an animal model of allergic contact dermatitis, a common pruritic disorder in humans
45 studied the role of cathelicidin in allergic contact dermatitis, a model requiring dendritic cells of
46 e confirmed the major findings in irritative contact dermatitis, a second model of cutaneous inflamma
47 owever, not all individuals develop allergic contact dermatitis (ACD) although they are regularly exp
48 llergens or irritants, resulting in allergic contact dermatitis (ACD) and/or irritant contact dermati
49 e sometimes encounter patients with allergic contact dermatitis (ACD) caused by EFCZ solution in our
50 role of the innate immune system in allergic contact dermatitis (ACD) has traditionally been confined
51          Atopic dermatitis (AD) and allergic contact dermatitis (ACD) have a dynamic relationship not
52 echanisms underlying elicitation in allergic contact dermatitis (ACD) have yet to be fully elucidated
53 tens is an efficient way to prevent allergic contact dermatitis (ACD) in mice.
54 the recent literature pertaining to allergic contact dermatitis (ACD) in the pediatric population.
55                                     Allergic contact dermatitis (ACD) is a common T-cell mediated inf
56                                     Allergic contact dermatitis (ACD) is a prevalent and poorly contr
57                                     Allergic contact dermatitis (ACD) is a pruritic skin disease caus
58                                     Allergic contact dermatitis (ACD) is classically described as a d
59                                     Allergic contact dermatitis (ACD) is the most common occupational
60                                     Allergic contact dermatitis (ACD) is well recognized as an advers
61                            Further, allergic contact dermatitis (ACD) model was used to evaluate the
62 skin permeation was investigated in allergic contact dermatitis (ACD) mouse model.
63 ressive to chronic, tumor-promoting allergic contact dermatitis (ACD) revealed how tumor-promoting ch
64 ls) in cellular infiltrate of human allergic contact dermatitis (ACD) skin challenge sites.
65 rritant contact dermatitis (ICD) or allergic contact dermatitis (ACD) that is sometimes clinically di
66 e evaluated the effect of OA-NO2 on allergic contact dermatitis (ACD) using an established model of c
67 ial role of Th2 responses in nickel allergic contact dermatitis (ACD) was demonstrated.
68 h in multiple preclinical models of allergic contact dermatitis (ACD), a pruritic inflammatory skin d
69                      Elicitation of allergic contact dermatitis (ACD), an inflammatory type 4 hyperse
70 ritant contact dermatitis (ICD) and allergic contact dermatitis (ACD), are common skin diseases.
71                    In many cases of allergic contact dermatitis (ACD), epidermal-resident memory CD8(
72 T (T(RM) ) cells are detrimental in allergic contact dermatitis (ACD), in which they contribute to th
73 mation are commonly associated with allergic contact dermatitis (ACD), it is not known if they are me
74              Using a mouse model of allergic contact dermatitis (ACD), we tested the effects of treat
75 immunologic similarities to chronic allergic contact dermatitis (ACD).
76 blocker (EC50=2 nM), could suppress allergic contact dermatitis (ACD).
77  in hair dye that is known to cause allergic contact dermatitis (ACD).
78 ic inflammatory diseases, including allergic contact dermatitis (ACD).
79 f SUCNR1/GPR91 expression mediating allergic contact dermatitis (ACD).
80 mory T (T(RM)) cells play a role in allergic contact dermatitis (ACD).
81  that IL-9 also has a role in human allergic contact dermatitis (ACD).
82 atitis (AD) as well as allergic and irritant contact dermatitis (ACD, ICD) are characterized by the s
83 by either inflammation alone (acute irritant contact dermatitis, acute allergic contact dermatitis) o
84                                     Allergic contact dermatitis affects 20% of children at some time
85 t SerpinB2(-/-) mice are more susceptible to contact dermatitis after topical application of dinitrof
86 ctions: food allergy, drug allergy, allergic contact dermatitis, allergic rhinitis and/or allergic co
87 hat MI can be an important cause of airborne contact dermatitis among painters and consumers.
88  pathogenesis of certain diseases, including contact dermatitis and allergy.
89 n and condition immune responses in irritant contact dermatitis and atopic dermatitis.
90              Certain skin disorders, such as contact dermatitis and chronic urticaria, are characteri
91                                     Allergic contact dermatitis and ICD were characterized by IFN-gam
92 ose association was also found with allergic contact dermatitis and increased specific IgE to Malasse
93 R agonists reduce inflammation in a model of contact dermatitis and inhibit inflammatory gene express
94 ganic chemical hapten which induces allergic contact dermatitis and is used in the treatment of warts
95                                     Allergic contact dermatitis and its animal model, contact hyperse
96 : endotoxin-induced toxic shock, PMA-induced contact dermatitis and lipopolysaccharide-induced ankle
97 rhinitis, asthma, and/or eczema in 38.2% and contact dermatitis and other eczema in 35.9%), and menta
98 12-myristate-13-acetate, a model of irritant contact dermatitis and oxazolone, a model of allergic co
99 hich NKT cells play a role, such as allergic contact dermatitis and psoriasis.
100 cals and may experience side effects such as contact dermatitis and skin irritation.
101  (n = 703) presenting with possible allergic contact dermatitis and subsequently undergoing patch tes
102 ondary outcomes included sources of allergic contact dermatitis and, for occupationally related cases
103 tly compromised, such as psoriasis, allergic contact dermatitis, and blistering disorders.
104 athogenesis of psoriasis, atopic dermatitis, contact dermatitis, and common autoimmune diseases.
105 es, including psoriasis, atopic and allergic contact dermatitis, and cutaneous T-cell lymphoma.
106  risk characteristics, incidence of allergic contact dermatitis, and incidence of wound complications
107 ng inflammatory events such as wound repair, contact dermatitis, and psoriasis.
108 ing chemicals in the development of allergic contact dermatitis, and suggest that the irritant effect
109 o strong levels in basal cells of psoriasis, contact dermatitis, and the proliferative cells of the a
110 ckground such as atopic dermatitis, allergic contact dermatitis, and urticaria are very common.
111 atory activity in both irritant and allergic contact dermatitis animal models.
112                       Given concerns such as contact dermatitis, antibiotic resistance, and healthcar
113                 Additional cases of allergic contact dermatitis are being reported with temporary hen
114               Atopic dermatitis and allergic contact dermatitis are both common skin diseases having
115 and human dermatological conditions, such as contact dermatitis, are discussed.
116  be applicable for the treatment of allergic contact dermatitis, are still largely unknown.
117 ed with either atopic dermatitis or allergic contact dermatitis as well as in an inducible mouse mode
118 pment of a spray to detect urushiol to avoid contact dermatitis, as well as to detect catecholamines
119 ay provide effective treatments for allergic contact dermatitis-associated chronic pruritus.
120 ent barrier abnormalities (subacute allergic contact dermatitis, atopic dermatitis), topical H1/2r ag
121 toxin C5a is a critical mediator of allergic contact dermatitis, bridging essential aspects of innate
122  is one of the most common forms of allergic contact dermatitis, but how the T-cell receptor (TCR) re
123 er defects might also predispose to allergic contact dermatitis by allowing greater penetration of ch
124 sis can be challenging because both types of contact dermatitis can appear similar by visual examinat
125         Herein, we report a case of allergic contact dermatitis caused by detergents containing CAPB,
126  Atopic dermatitis (AD), psoriasis (PS), and contact dermatitis (CD) are common skin diseases, charac
127                                     Allergic contact dermatitis (CD) is a chronic inflammatory skin d
128                                              Contact dermatitis (CD) is among the most common inflamm
129                                              Contact dermatitis (CD), including allergic and irritant
130 ribe the histopathological features of acute contact dermatitis (CD).
131  may induce an inflammatory disease known as contact dermatitis (CD).
132 EGs were found between allergic and irritant contact dermatitis CHE.
133 rA3(+) neurons under both naive and allergic contact dermatitis conditions.
134        We report 7 cases of erosive irritant contact dermatitis due to chlorhexidine gluconate-impreg
135       We diagnosed the patient with allergic contact dermatitis due to the EITC and BITC present in n
136  observed seem to be in most cases 'systemic contact dermatitis' due to oral or parenteral re-exposur
137  a better understanding of the complexity of contact dermatitis, especially ACD-a disease that may be
138 -) mice are predisposed to mount an allergic contact dermatitis, especially at hapten threshold level
139 suffering from psoriasis, atopic or allergic-contact dermatitis express CCR10.
140 e cross-sectional analysis of North American Contact Dermatitis Group (NACDG) data from multiple cent
141 ngredients represented in the North American Contact Dermatitis Group (NACDG) series were conducted u
142 rom 3 tertiary care sites of the Mayo Clinic Contact Dermatitis Group and a total of 5943 patients we
143  a retrospective analysis of the Mayo Clinic Contact Dermatitis Group corticosteroid patch test data
144    Clinical scoring using the North American Contact Dermatitis Group method was also performed.
145        Patch testing used the North American Contact Dermatitis Group standard series.
146 his retrospective analysis of North American Contact Dermatitis Group, European Surveillance System o
147          The role of MCs in chronic allergic contact dermatitis has not been investigated, in part be
148  past decade, mechanisms underlying allergic contact dermatitis have been intensively investigated by
149 le for nitrile rubber glove-induced allergic contact dermatitis have not been fully elucidated.
150 ream included folliculitis, nasopharyngitis, contact dermatitis, headache, upper respiratory tract in
151 tes, especially during allergic and irritant contact dermatitis, however, is less well understood.
152  Atopic dermatitis (AD), as well as irritant contact dermatitis (ICD) and allergic contact dermatitis
153                                     Irritant contact dermatitis (ICD) is caused by direct damage to t
154 tients, there is often a coexisting irritant contact dermatitis (ICD) or allergic contact dermatitis
155 sible for the signs and symptoms of irritant contact dermatitis (ICD).
156   In addition, AFC inhibits in vivo allergic contact dermatitis in a mouse model utilizing sensitizat
157             The documented rates of allergic contact dermatitis in children are on the rise.
158 logy and clinical manifestations of allergic contact dermatitis in children.
159 markers to distinguish allergic and irritant contact dermatitis in human skin.
160 the recent literature pertaining to allergic contact dermatitis in the pediatric population.
161 ically applied THC on DNFB-mediated allergic contact dermatitis in wild-type and CB1/2 receptor-defic
162                     In contrast to classical contact dermatitis, in which myeloid dendritic cells sen
163 The most represented forms of non-eczematous contact dermatitis include the erythema multiforme-like,
164 ice show a stronger inflammation in allergic contact dermatitis, indicating a regulatory role of CD16
165 had no effect on croton oil-induced irritant contact dermatitis, indicating that morphine's effects o
166  prolonged itch in a mouse model of allergic contact dermatitis induced by squaric acid dibutylester.
167 d dyskeratosis follicularis Darier, allergic contact dermatitis, infectious folliculitis, varicella z
168                             In patients with contact dermatitis, inflammasome-mediated IL-1 activatio
169                                     Allergic contact dermatitis is a chronic T cell-driven inflammato
170                                              Contact dermatitis is a common disease that is caused by
171                                     Allergic contact dermatitis is a common disorder that has fascina
172                                     Allergic contact dermatitis is a common inflammatory skin disease
173                                     Allergic contact dermatitis is a common skin disease associated w
174                                      Erosive contact dermatitis is an under-recognized complication o
175                                     Allergic contact dermatitis is commonly associated with exposure
176 t of new drugs for personalized treatment of contact dermatitis is considerable.
177 ide support for the hypothesis that allergic contact dermatitis is not a classic delayed type hyperse
178                                     Allergic contact dermatitis is one of the most common occupationa
179                                     Allergic contact dermatitis is the most frequent occupational dis
180                                              Contact dermatitis is the result of inflammatory respons
181 chanism in those who do not develop allergic contact dermatitis is tolerance induction by repeated ex
182 ally induced skin sensitization, or allergic contact dermatitis, is a common occupational and public
183 own to cause skin rash, dermal inflammation, contact dermatitis, leucoderma, and cancer promotion.
184   Women are more likely to have occupational contact dermatitis, mainly due to wet work.
185                                     Allergic contact dermatitis may affect as many as 20% of the pedi
186 ave suggested that chemical-induced allergic contact dermatitis may not be a traditional type IV hype
187 EC on T-cell extravasation using an allergic contact dermatitis model in mice.
188 iscontinued therapy because of side effects (contact dermatitis [n = 2], nausea [n = 1], and acute pa
189                      Nickel-induced allergic contact dermatitis (nACD) remains a major occupational s
190                                     Allergic contact dermatitis occurs less frequently in the first f
191 e PPD-related ACD and 7 hairdressers without contact dermatitis on day 4 after patch testing with 1%
192  have significantly higher rates of allergic contact dermatitis on the face.
193  irritant contact dermatitis, acute allergic contact dermatitis) or by prominent barrier abnormalitie
194 ved in sensory neurons of mice with allergic contact dermatitis- or dry skin-elicited itch; however,
195                        Using human skin from contact dermatitis patients and a mouse model of CHS, we
196                   Not infrequently, however, contact dermatitis presents with noneczematous features.
197  agonists in models of irritant and allergic contact dermatitis produced in mouse ears by topical tre
198                                          The contact dermatitis rate was 1.1% with and 0.29% without
199 d inflammation in human skin resembles acute contact dermatitis rather than psoriasis.
200           Furthermore, allergic and irritant contact dermatitis reactions were exaggerated in FVB.del
201 pite a trend toward weaker clinical allergic contact dermatitis reactions.
202  CD39 deficiency in irritant versus allergic contact dermatitis, reflecting its diverse roles in regu
203               To use data from the Pediatric Contact Dermatitis Registry to elucidate the association
204  clinical phenotype of irritant and allergic contact dermatitis remains challenging.
205 eries and additional PT series of the German Contact Dermatitis Research Group (DKG) and (ii) charact
206 ) 2, 3, and 7 according to the International Contact Dermatitis Research Group criteria.
207 that was not clinically infected and was not contact dermatitis, seborrheic eczema or hand eczema.
208 or fragrances were derived from the American Contact Dermatitis Society's Contact Allergen Management
209                                     Allergic contact dermatitis, such as in response to poison ivy or
210      In a well-established model of allergic contact dermatitis, the absence of Mincle leads to a sig
211 tory responses in a mouse model for allergic contact dermatitis, the contact hypersensitivity (CHS) r
212  chlorhexidine gluconate is a known cause of contact dermatitis, the phenotypic range of this adverse
213                   The prevalence of allergic contact dermatitis to allergens (eg, fragrance) is highe
214 dy we use an in vivo mouse model of allergic contact dermatitis to investigate how nanoparticles (NPs
215                       Prevalence of allergic contact dermatitis to MCI/MI and MI.
216                    Individuals with allergic contact dermatitis to one topical corticosteroid may als
217 ed aluminium tubes pose a risk of developing contact dermatitis to patients sensitized to ER based on
218 idil for patients with a history of allergic contact dermatitis to topical minoxidil, the long-term s
219 frequency of DNCB sensitization and allergic contact dermatitis to topically applied mechlorethamine
220                                              Contact dermatitis tremendously impacts the quality of l
221                                Additionally, contact dermatitis, urticaria, and drug reactions are ad
222 esis of rosacea, atopic dermatitis, allergic contact dermatitis, urticaria, and mastocytosis.
223                         Irritant or allergic contact dermatitis usually presents as an eczematous pro
224 up using white petrolatum developed allergic contact dermatitis vs 4 patients (0.9%) in the group usi
225 lly, chronic itch from DNFB-induced allergic contact dermatitis was decreased by Oprm1-Vgat deletion.
226                                  The rate of contact dermatitis was similar (0.5% vs. 0.5%; P = 1.00)
227 r and cellular mechanism underlying allergic contact dermatitis, we evaluated oxazolone-induced chang
228 osts of chlorhexidine-impregnated sponge and contact dermatitis were calculated prospectively using m
229 de of either 691.8 (AD) or 692.9 (eczema and contact dermatitis) were queried.
230 sensitivity reactions, resulting in allergic contact dermatitis, which clinically resembles eczema.
231  participants presented with mild irritative contact dermatitis, which had disappeared by the 1-week
232          In human subjects imiquimod induces contact dermatitis with the distinctive feature that pDC
233 t frequent cause of T cell-mediated allergic contact dermatitis worldwide.

 
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