Alopecia areata profiling shows TH1, TH2, and IL-23 cytokine activation without parallel TH17/TH22 skewing.
💡 한 문장 핵심
원형 탈모 프로파일링에서 나타난 TH1, TH2, IL-23 사이토카인 활성화와 TH17/TH22 편향의 부재
5/5 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
🇰🇷 한글 요약 🌐 Abstract
【연구 목적】
원형 탈모증(alopecia areata, AA) 두피 조직의 사이토카인 경로 분자 프로파일을 규명하고, 아토피피부염(atopic dermatitis, AD) 및 건선(psoriasis)과 비교하는 것이 목적입니다. 기존 연구가 TH1/IFN-γ 반응에 집중된 것과 달리, AA와 아토피의 공유 유전 배경을 함께 검증하고자 했습니다.
【방법】
AA 환자의 병변 두피 27개·비병변 17개 검체를 정상 두피(n=6)와 비교해 마이크로어레이 및 RT-PCR 발현 분석을 시행했습니다. AA 유전자 발현을 AD·건선 검체와도 비교했으며, 차등발현유전자(DEG)는 fold change 1.5 초과, FDR 0.05 미만 기준을 적용했습니다.
【주요 결과】
AA 병변에서 면역 유전자는 상향, 모발 케라틴 유전자(KRT86, KRT85)는 유의하게 하향 조절되었습니다. TH1/인터페론(IFNG, CXCL10/CXCL9)뿐 아니라 TH2(IL13, periostin 등), TH9/IL-9, IL-23(p40·p19) 경로도 함께 활성화된 반면, TH17/TH22 마커 증가는 없었습니다. 두피 침범 범위가 25%를 넘으면 면역·케라틴 이상과 비병변부 이상(CXCL10, KRT85)도 더 컸습니다.
【임상적 시사점 (성형외과 의사 관점)】
AA는 단일 경로가 아닌 TH2·TH1·IL-23·TH9 복합 활성으로, 모발이식·두피 시술 전 활동성 AA 환자에서는 면역학적 활성을 고려해야 합니다. 향후 항-TH2, 항-TH1, 항-IL-23 표적치료가 모발 재생 보조 전략이 될 수 있어, 탈모 상담 시 단순 국소치료를 넘어선 표적 약제 가능성을 염두에 둘 가치가 있습니다.
[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
【연구 목적】 원형 탈모증(alopecia areata, AA) 두피 조직의 사이토카인 경로 분자 프로파일을 규명하고, 아토피피부염(atopic dermatitis, AD) 및 건선(psoriasis)과 비교하는 것이 목적입니다.
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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- Molecular signatures define alopecia areata subtypes and transcriptional biomarkers.
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- 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.
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