Alopecia areata profiling shows TH1, TH2, and IL-23 cytokine activation without parallel TH17/TH22 skewing.
4/5 보강
TL;DR
The data associate the AA signature with TH2, TH1, IL-23, and IL-9/TH9 cytokine activation, suggesting consideration of anti-TH2, anti-Th1, and anti-IL-23 targeting strategies.
PICO 자동 추출 (휴리스틱, conf 2/4)
유사 논문P · Population 대상 환자/모집단
환자: AA for comparison with normal scalp samples (n = 6)
I · Intervention 중재 / 시술
추출되지 않음
C · Comparison 대조 / 비교
추출되지 않음
O · Outcome 결과 / 결론
[CONCLUSIONS] Our data associate the AA signature with TH2, TH1, IL-23, and IL-9/TH9 cytokine activation, suggesting consideration of anti-TH2, anti-TH1, and anti-IL-23 targeting strategies. Similar to psoriasis and AD, clinical trials with selective antagonists are required to dissect key pathogenic pathways.
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연도별 인용 (2015–2026) · 합계 250
OpenAlex 토픽 ·
Hair Growth and Disorders
Dermatology and Skin Diseases
Psoriasis: Treatment and Pathogenesis
Abstract 🌐 Abstract
[BACKGROUND] Alopecia areata (AA) is a common T cell-mediated disorder with limited therapeutics. A molecular profile of cytokine pathways in AA tissues is lacking. Although studies have focused on TH1/IFN-γ responses, several observations support a shared genetic background between AA and atopy.
[OBJECTIVE] We sought to define the AA scalp transcriptome and associated biomarkers with comparisons with atopic dermatitis (AD) and psoriasis.
[METHODS] We performed microarray and RT-PCR profiling of 27 lesional and 17 nonlesional scalp samples from patients with AA for comparison with normal scalp samples (n = 6). AA gene expression was also compared with samples from patients with lesional or nonlesional AD and those with psoriasis. A fold change of greater than 1.5 and a false discovery rate of less than 0.05 were used for differentially expressed genes (DEGs).
[RESULTS] We established the AA transcriptomes (lesional vs nonlesional: 734 DEGs [297 upregulated and 437 downregulated]; lesional vs normal: 4230 DEGs [1980 upregulated and 2250 downregulated]), including many upregulated immune and downregulated hair keratin genes. Equally impressive as upregulation in TH1/interferon markers (IFNG and CXCL10/CXCL9) were those noted in TH2 (IL13, CCL18, CCL26, thymic stromal lymphopoietin, and periostin), TH9/IL-9, IL-23 (p40 and p19), and IL-16 mediators (all P < .05). There were no increases in TH17/TH22 markers. Hair keratin (KRT) expressions (ie, KRT86 and KRT85) were significantly suppressed in lesional skin. Greater scalp involvement (>25%) was associated with greater immune and keratin dysregulation and larger abnormalities in nonlesional scalp samples (ie, CXCL10 and KRT85).
[CONCLUSIONS] Our data associate the AA signature with TH2, TH1, IL-23, and IL-9/TH9 cytokine activation, suggesting consideration of anti-TH2, anti-TH1, and anti-IL-23 targeting strategies. Similar to psoriasis and AD, clinical trials with selective antagonists are required to dissect key pathogenic pathways.
[OBJECTIVE] We sought to define the AA scalp transcriptome and associated biomarkers with comparisons with atopic dermatitis (AD) and psoriasis.
[METHODS] We performed microarray and RT-PCR profiling of 27 lesional and 17 nonlesional scalp samples from patients with AA for comparison with normal scalp samples (n = 6). AA gene expression was also compared with samples from patients with lesional or nonlesional AD and those with psoriasis. A fold change of greater than 1.5 and a false discovery rate of less than 0.05 were used for differentially expressed genes (DEGs).
[RESULTS] We established the AA transcriptomes (lesional vs nonlesional: 734 DEGs [297 upregulated and 437 downregulated]; lesional vs normal: 4230 DEGs [1980 upregulated and 2250 downregulated]), including many upregulated immune and downregulated hair keratin genes. Equally impressive as upregulation in TH1/interferon markers (IFNG and CXCL10/CXCL9) were those noted in TH2 (IL13, CCL18, CCL26, thymic stromal lymphopoietin, and periostin), TH9/IL-9, IL-23 (p40 and p19), and IL-16 mediators (all P < .05). There were no increases in TH17/TH22 markers. Hair keratin (KRT) expressions (ie, KRT86 and KRT85) were significantly suppressed in lesional skin. Greater scalp involvement (>25%) was associated with greater immune and keratin dysregulation and larger abnormalities in nonlesional scalp samples (ie, CXCL10 and KRT85).
[CONCLUSIONS] Our data associate the AA signature with TH2, TH1, IL-23, and IL-9/TH9 cytokine activation, suggesting consideration of anti-TH2, anti-TH1, and anti-IL-23 targeting strategies. Similar to psoriasis and AD, clinical trials with selective antagonists are required to dissect key pathogenic pathways.
- 표본수 (n) 6
- p-value P < .05
The data associate the AA signature with TH2, TH1, IL-23, and IL-9/TH9 cytokine activation, suggesting consideration of anti-TH2, anti-Th1, and anti-IL-23 targeting strategies.
APA 7
M, S., Ungar, B., Noda, S., Shroff, A., Mansouri, Y., Fuentes-Duculan, J., Czernik, A., Zheng, X., Estrada, Y. D., Xu, H., Peng, X., Shemer, A., Krueger, J. G., Lebwohl, M. G., & Guttman-Yassky, E. (2015). Alopecia areata profiling shows th1, th2, and il-23 cytokine activation without parallel th17/th22 skewing.. The Journal of allergy and clinical immunology, 136(5), 1277-87. https://doi.org/10.1016/j.jaci.2015.06.032
Vancouver
M S, Ungar B, Noda S, Shroff A, Mansouri Y, Fuentes-Duculan J, et al. Alopecia areata profiling shows TH1, TH2, and IL-23 cytokine activation without parallel TH17/TH22 skewing. Jour. alle. clin. immu.. 2015;136(5):1277-87. doi:10.1016/j.jaci.2015.06.032
AMA 11
M S, Ungar B, Noda S, Shroff A, Mansouri Y, Fuentes-Duculan J, et al. Alopecia areata profiling shows TH1, TH2, and IL-23 cytokine activation without parallel TH17/TH22 skewing. Jour. alle. clin. immu.. 2015;136(5):1277-87. doi:10.1016/j.jaci.2015.06.032
Chicago
M, S., Ungar, B., Noda, S., Shroff, A., Mansouri, Y., Fuentes-Duculan, J., Czernik, A., Zheng, X., Estrada, Y. D., Xu, H., and .... 2015. "Alopecia areata profiling shows TH1, TH2, and IL-23 cytokine activation without parallel TH17/TH22 skewing." The Journal of allergy and clinical immunology 136 (5): 1277-87. https://doi.org/10.1016/j.jaci.2015.06.032
MLA 9
M, S., et al. "Alopecia areata profiling shows TH1, TH2, and IL-23 cytokine activation without parallel TH17/TH22 skewing." The Journal of allergy and clinical immunology, vol. 136, no. 5, 2015, pp. 1277-87. doi:10.1016/j.jaci.2015.06.032.
PMID
26316095 ↗
추출된 의학 개체 (NER)
해부
두피 scalp
×5
전체 NER 표 보기
| 유형 | 영어 표현 | 한국어 / 풀이 | UMLS CUI | 출처 | 등장 |
|---|---|---|---|---|---|
| 해부 | scalp
|
두피 | dict | 5 | |
| 질환 | alopecia areata
|
원형 탈모증 | dict | 2 |
🏷️ 키워드 / MeSH 📖 같은 키워드 OA만
- Adult
- Alopecia Areata
- Biomarkers
- Chemokines
- Dermatitis
- Atopic
- Female
- Humans
- Interleukin-23
- Keratins
- Hair-Specific
- Lymphocyte Activation
- Male
- Microarray Analysis
- Middle Aged
- Psoriasis
- Th1 Cells
- Th2 Cells
- Transcriptome
- Young Adult
- Alopecia areata
- IL-23
- T(H)1
- T(H)2
… 외 3개
인용 관계
그래프 OA 노드: 5/8 (63%)
· 참조 0편 · 후속 5편
이 논문을 인용한 후속 연구 20
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- Alopecia areata: a review on diagnosis, immunological etiopathogenesis and treatment options.
- Phase 2a randomized clinical trial of dupilumab (anti-IL-4Rα) for alopecia areata patients.
- Molecular signatures define alopecia areata subtypes and transcriptional biomarkers.
- Lifestyle Factors Involved in the Pathogenesis of Alopecia Areata.
- The Role of Serum Th1, Th2, and Th17 Cytokines in Patients with Alopecia Areata: Clinical Implicatio…
- Alopecia Areata: Current Treatments and New Directions.
- The Changing Landscape of Alopecia Areata: The Therapeutic Paradigm.
- Alopecia Areata: An Autoimmune Disease of Multiple Players.
- Scalp biomarkers during dupilumab treatment support Th2 pathway pathogenicity in alopecia areata.
- The current state of knowledge of the immune ecosystem in alopecia areata.
- Understanding autoimmunity of vitiligo and alopecia areata.
- Deciphering the Complex Immunopathogenesis of Alopecia Areata.
- New and Emerging Therapies for Alopecia Areata.
- Drug-induced alopecia after dupilumab therapy.
- Transient Efficacy of Tofacitinib in Alopecia Areata Universalis.
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