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CD80CD86 deficiency disrupts regulatory CD4+FoxP3+T cell homoeostasis and induces autoimmune-like alopecia.
Exp Dermatol. 2017 11; 26(11):1053-1059.ED

Abstract

Alopecia areata (AA) is an autoimmune disease that results in spot baldness in humans. Adequate animal models for AA are currently lacking. The objective of this study was to elucidate the mechanism of autoimmune-like alopecia (ALA) in C57BL/6.CD80CD86-deficient (B6.CD80CD86[-/-]) mice. Incidence and severity of alopecia were analysed in 58 B6.CD80CD86[-/-] mice using histological examination, flow cytometry, multiplex enzyme-linked immunosorbent assay, quantitative RT-PCR and CD25 inhibition test. Both male and female B6.CD80CD86[-/-] mice showed almost 100% incidence of hair loss at 40 weeks of age. Moreover, CD4+FoxP3+Treg (Treg) cell population in B6.CD80CD86[-/-] mice was significantly lower than in B6 mice, which presumably underlined autoimmune reaction. Histologically, B6.CD80CD86[-/-] mice showed CD4+ and CD8+ T-cell infiltration around terminal follicle region and exhibited hair follicle destruction in the anagen or catagen stage. Negative correlation between the number of CD4+FoxP3+ Tregs and ALA was confirmed by the CD25 depletion test in B6 mice, as follicle destruction was similar to that observed in B6.CD80CD86[-/-] animals. CD80CD86 deficiency disrupted CD4+FoxP3+ Treg homoeostasis and prompted the development of ALA. We demonstrated that B6.CD80CD86[-/-] mice might have several advantages as an ALA model, because they exhibited high incidence of disease phenotype and epipathogenesis similar to that observed in human AA.

Authors+Show Affiliations

Designed Animal and Transplantation Research Institute, Greenbio Research and Technology, Seoul National University, Pyeongchang, Kangwon, Korea.Designed Animal and Transplantation Research Institute, Greenbio Research and Technology, Seoul National University, Pyeongchang, Kangwon, Korea.Graduate School of International Agricultural Technology, Seoul National University, Pyeongchang, Kangwon, Korea.Graduate School of International Agricultural Technology, Seoul National University, Pyeongchang, Kangwon, Korea.Graduate School of International Agricultural Technology, Seoul National University, Pyeongchang, Kangwon, Korea.Institute of Endemic Diseases, Seoul National University College of Medicine, Seoul, Korea. Xenotransplantation Research Center, Seoul National University, Chongno, Seol, Korea.Designed Animal and Transplantation Research Institute, Greenbio Research and Technology, Seoul National University, Pyeongchang, Kangwon, Korea. Graduate School of International Agricultural Technology, Seoul National University, Pyeongchang, Kangwon, Korea.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

28423200

Citation

Bae, Ji-Hyun, et al. "CD80CD86 Deficiency Disrupts Regulatory CD4+FoxP3+T Cell Homoeostasis and Induces Autoimmune-like Alopecia." Experimental Dermatology, vol. 26, no. 11, 2017, pp. 1053-1059.
Bae JH, Hwang WS, Jang YJ, et al. CD80CD86 deficiency disrupts regulatory CD4+FoxP3+T cell homoeostasis and induces autoimmune-like alopecia. Exp Dermatol. 2017;26(11):1053-1059.
Bae, J. H., Hwang, W. S., Jang, Y. J., Lee, Y. H., Jang, D. E., Kim, J. S., & Yeom, S. C. (2017). CD80CD86 deficiency disrupts regulatory CD4+FoxP3+T cell homoeostasis and induces autoimmune-like alopecia. Experimental Dermatology, 26(11), 1053-1059. https://doi.org/10.1111/exd.13371
Bae JH, et al. CD80CD86 Deficiency Disrupts Regulatory CD4+FoxP3+T Cell Homoeostasis and Induces Autoimmune-like Alopecia. Exp Dermatol. 2017;26(11):1053-1059. PubMed PMID: 28423200.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - CD80CD86 deficiency disrupts regulatory CD4+FoxP3+T cell homoeostasis and induces autoimmune-like alopecia. AU - Bae,Ji-Hyun, AU - Hwang,Woo-Sung, AU - Jang,Yoo-Jin, AU - Lee,Yoon-Hoo, AU - Jang,Da-Eun, AU - Kim,Jung-Sik, AU - Yeom,Su-Cheong, Y1 - 2017/07/03/ PY - 2017/04/13/accepted PY - 2017/4/20/pubmed PY - 2018/7/22/medline PY - 2017/4/20/entrez KW - CD4+FoxP3+Treg KW - CD80CD86 KW - autoimmune-like alopecia SP - 1053 EP - 1059 JF - Experimental dermatology JO - Exp Dermatol VL - 26 IS - 11 N2 - Alopecia areata (AA) is an autoimmune disease that results in spot baldness in humans. Adequate animal models for AA are currently lacking. The objective of this study was to elucidate the mechanism of autoimmune-like alopecia (ALA) in C57BL/6.CD80CD86-deficient (B6.CD80CD86[-/-]) mice. Incidence and severity of alopecia were analysed in 58 B6.CD80CD86[-/-] mice using histological examination, flow cytometry, multiplex enzyme-linked immunosorbent assay, quantitative RT-PCR and CD25 inhibition test. Both male and female B6.CD80CD86[-/-] mice showed almost 100% incidence of hair loss at 40 weeks of age. Moreover, CD4+FoxP3+Treg (Treg) cell population in B6.CD80CD86[-/-] mice was significantly lower than in B6 mice, which presumably underlined autoimmune reaction. Histologically, B6.CD80CD86[-/-] mice showed CD4+ and CD8+ T-cell infiltration around terminal follicle region and exhibited hair follicle destruction in the anagen or catagen stage. Negative correlation between the number of CD4+FoxP3+ Tregs and ALA was confirmed by the CD25 depletion test in B6 mice, as follicle destruction was similar to that observed in B6.CD80CD86[-/-] animals. CD80CD86 deficiency disrupted CD4+FoxP3+ Treg homoeostasis and prompted the development of ALA. We demonstrated that B6.CD80CD86[-/-] mice might have several advantages as an ALA model, because they exhibited high incidence of disease phenotype and epipathogenesis similar to that observed in human AA. SN - 1600-0625 UR - https://www.unboundmedicine.com/medline/citation/28423200/CD80CD86_deficiency_disrupts_regulatory_CD4+FoxP3+T_cell_homoeostasis_and_induces_autoimmune_like_alopecia_ DB - PRIME DP - Unbound Medicine ER -