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1 T cell-mediated hair loss disease (alopezia areata).
2 whereas 39 of 44 controls developed alopecia areata.
3 didate genes in the pathogenesis of alopecia areata.
4 ing the use of these treatments for alopecia areata.
5 similar to those observed in human alopecia areata.
6 erstanding of the genetic basis for alopecia areata.
7 for decubitus ulcer, and 0.01% for alopecia areata.
8 d arthritis, atopic dermatitis, and alopecia areata.
9 e treatment of warts, melanoma, and alopecia areata.
10 vancing the therapeutic pipeline of alopecia areata.
11 juvenile idiopathic arthritis, and alopecia areata.
12 tients aged 12 years and older with alopecia areata.
13 mation that targets anagen hairs in alopecia areata.
14 kinase inhibitor, in patients with alopecia areata.
15 tive, SCD-153, for the treatment of alopecia areata.
16 being explored for the treatment of alopecia areata.
17 agent for limited patchy childhood alopecia areata.
18 igh-incidence model for spontaneous alopecia areata.
19 s a key step in the pathogenesis of alopecia areata.
20 buting factor in the development of alopecia areata.
21 fluvium, androgenetic alopecia, and alopecia areata.
22 s potentially associated with human alopecia areata.
23 C57BL/6J mice do not develop alopecia areata.
24 ng this locus as being important in alopecia areata.
25 he IL-1RN and various phenotypes of alopecia areata.
26 n grafts from mice with spontaneous alopecia areata.
27 ic inflammatory diseases, including alopecia areata.
28 atitis, 0.97 (95% CI, 0.65-1.46) in alopecia areata, 0.90 (95% CI, 0.49-1.65) in vitiligo, 1.64 (95%
29 1.83 in atopic dermatitis, 0.94 in alopecia areata, 0.93 in vitiligo, 1.65 in HS and 1.53 in CISD ov
30 lymphoma (1.85[1.66-2.06], RD0.02), Alopecia Areata (1.77[1.71-1.83], RD0.2), Crohn's disease (1.62[1
33 ic alopecia (37.3 128.4, 46.1]) and alopecia areata (24.9 [17.2, 32.6]) were statistically significan
34 pic dermatitis [2.46 (2.40, 2.53)], alopecia areata [3.47 (3.24, 3.71)], contact dermatitis [1.92 (1.
35 We aimed to determine the risk of alopecia areata (AA) and vitiligo associated with atopic dermatit
43 g been appreciated that episodes of alopecia areata (AA) have occurred after severely stressful life
44 universalis is an uncommon form of alopecia areata (AA) involving hair loss over the entire scalp an
65 Characterizing blood profile of alopecia areata (AA) is important not only for treatment advancem
68 y investigated frontiers in current alopecia areata (AA) pathobiology research, with an emphasis on p
73 dermatitis (AD) among patients with alopecia areata (AA) using data from the Merative MarketScan Rese
75 m both humans and C3H/HeJ mice with alopecia areata (AA), a T cell-mediated autoimmune disease of the
77 uraging results in the treatment of alopecia areata (AA), an autoimmune form of hair loss, in small,
78 ety and depression in patients with alopecia areata (AA), as well as a positive association of AA wit
79 ype 1 (ILC1) in the pathogenesis of alopecia areata (AA), because we found them to be significantly i
80 patients under TNFi therapy develop alopecia areata (AA), the most common inflammatory hair loss dise
88 5, and July 1, 2020, using keywords alopecia areata, acne, atopic dermatitis, lichen planus, psoriasi
92 lus, but only lymph node cells from alopecia areata affected mice displayed an increased response wit
93 s, lymph node and spleen cells from alopecia areata affected mice injected into normal haired litterm
94 4+ CD8+ expressing cells in chronic alopecia areata affected mice using monoclonal antibodies permitt
96 ll-mediated autoimmune disease, but alopecia areata affected skin graft hosts may resist alopecia are
98 a, only two of 22 receiving further alopecia areata affected skin grafts developed alopecia areata, w
99 s clinic, 2 to 16 years of age with alopecia areata affecting at least 10% of scalp surface area, wer
102 For comparison, skin biopsies from alopecia areata and androgenetic alopecia affected humans were al
103 tients aged 12 years and older with alopecia areata and at least 50% scalp hair loss were randomly as
104 peutic techniques for patients with alopecia areata and further refine which subtypes of the disease
106 disease, thyroid disease, vitiligo, alopecia areata and inflammatory bowel disease) were self-reporte
108 , in which the outcome variable was alopecia areata and the main predictor was natural hair color bef
109 g psoriasis, atopic dermatitis, and alopecia areata) and eight other immune-mediated diseases and obt
111 atosus, Sjogren syndrome, vitiligo, alopecia areata, and multiple sclerosis) and each individual auto
113 ditions, such as atopic dermatitis, alopecia areata, and vitiligo, but there is a current US Food and
114 dominantly acne, atopic dermatitis, alopecia areata, and vitiligo, only 27.0% had T scores less than
115 itiligo," "seborrheic dermatitis," "alopecia areata," and "lichen planus." Diverse study populations
116 es of 110 patients and 45 controls: alopecia areata, ankylosing spondylitis, dermatomyositis, Graves'
119 observed between IL-1RN and patchy alopecia areata but it was not statistically significant (p =0.06
120 J mouse skin to littermates induces alopecia areata, but high dietary soy oil reduces alopecia areata
122 t 2% of people over their lifetime, alopecia areata can present with a range of clinical features, fr
123 en atopic dermatitis, vitiligo, and alopecia areata, challenging previously established notions of th
124 s exhibited significantly decreased alopecia areata compared with those with light brown hair (aOR, 0
125 downregulated during onset of mouse alopecia areata consistent with an inflammatory cell-mediated dis
126 psoriasis, acne vulgaris, pruritus, alopecia areata, decubitus ulcer, urticaria, scabies, fungal skin
127 rds the graft, it is suggested that alopecia areata develops as a consequence of an inappropriate imm
128 successfully identify a significant Alopecia Areata disease-relevant gene, KRT82, and reveal a propos
133 was distributed using the National Alopecia Areata Foundation (NAAF) with the aim of assessing (1) p
134 C3H/HeJ mice spontaneously develop alopecia areata from 5 mo of age and older in females and later i
136 healthy controls and patients with alopecia areata, identifying diverse cell types of the hair folli
137 st treatment for adults with severe alopecia areata in 2022 and for adolescents with severe alopecia
138 022 and for adolescents with severe alopecia areata in 2023, with multiple investigational treatments
139 rize a new high-incidence model for alopecia areata in C57BL/6J mice, the first to our knowledge to a
141 (+) T effector memory cells mediate alopecia areata in part through Janus kinase (JAK) signaling and
142 be a suitable treatment option for alopecia areata in patients who are candidates for systemic thera
143 port a previously proposed model of alopecia areata in which immunity is directed against melanogenes
144 tis, inflammatory bowel disease and alopecia areata, in which stimulation of innate immunity activate
145 amaging variants in 51 heterozygous Alopecia Areata individuals (6.01%), achieving genome-wide signif
146 Consensus was reached that the Alopecia Areata Investigator Global Assessment scale adequately c
161 control study seem to indicate that alopecia areata is modulated by natural hair color, preferentiall
166 8), atopic dermatitis (n = 30 418), alopecia areata (n = 17 889), vitiligo (n = 7735), or HS (n = 593
167 0), androgenetic alopecia (n = 52), alopecia areata (n = 17), and alopecia areata totalis/universalis
171 d skin grafts but failed to develop alopecia areata, only two of 22 receiving further alopecia areata
173 ffected skin graft hosts may resist alopecia areata onset through active counter-regulatory mechanism
174 the contribution from mild cases of alopecia areata [OR 1.48 (0.96, 2.29)], suggesting that IL-1 alph
176 cell-mediated disease mechanism in alopecia areata pathogenesis and suggested targeting antigen-pres
181 a Areata Quality of Life Index, and Alopecia Areata Patients' Quality of Life) were AA-specific healt
182 syndrome, Crohn disease, vitiligo, alopecia areata, pernicious anemia, ulcerative colitis, rheumatoi
185 Treatment reduced skin pathology in alopecia areata, psoriasis, and atopic dermatitis, while decreasi
186 (Scale of Alopecia Areata Distress, Alopecia Areata Quality of Life Index, and Alopecia Areata Patien
193 Patient Priority Outcomes [AAPPO], Alopecia Areata Severity Self-Assessment, and Alopecia Areata Sym
195 d resistance locus) did not develop alopecia areata, supporting this locus as being important in alop
197 reata Severity Self-Assessment, and Alopecia Areata Symptom Impact Scale) were based on both construc
198 diseases, ranging from psoriasis to alopecia areata to vitiligo to lupus erythematosus to atopic derm
199 have been reported in patients with alopecia areata totalis (AT) or universalis (AU), the most severe
200 effluvium (50.1 [33.9, 66.33]) and alopecia areata totalis/universalis (52.3 [23.1, 81.5]) were not
204 ntify rare variants contributing to Alopecia Areata using a whole exome sequencing and gene-level bur
206 orded psoriasis, atopic dermatitis, alopecia areata, vitiligo, or hidradenitis suppurativa were inclu
207 of dermatological diseases such as alopecia areata, vitiligo, psoriasis and atopic dermatitis, commo
212 gate the role of the IL-1 system in alopecia areata we examined three biallelic polymorphisms within
213 pruritus, scabies, cellulitis, and alopecia areata were underrepresented in CDSR when matched with c
215 eata affected skin grafts developed alopecia areata, whereas 39 of 44 controls developed alopecia are
216 ng these individuals, 1673 cases of alopecia areata with reported hair color were captured and matche
217 terized by loss of hair in patches (alopecia areata) with progression in some individuals to total lo