勘误：骨髓来源的抑制性细胞外泌体在自身免疫性斑秃小鼠模型中的免疫调节作用。
Erratum: Immunoregulatory Effects of Myeloid-Derived Suppressor Cell Exosomes in Mouse Model of Autoimmune Alopecia Areata.
出版信息
Front Immunol. 2021 Dec 24;12:832980. doi: 10.3389/fimmu.2021.832980. eCollection 2021.
Abstract
[This corrects the article DOI: 10.3389/fimmu.2018.01279.].
摘要
[本文更正了文章的数字对象标识符：10.3389/fimmu.2018.01279。]
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Erratum: Immunoregulatory Effects of Myeloid-Derived Suppressor Cell Exosomes in Mouse Model of Autoimmune Alopecia Areata.勘误：骨髓来源的抑制性细胞外泌体在自身免疫性斑秃小鼠模型中的免疫调节作用。
Front Immunol. 2021 Dec 24;12:832980. doi: 10.3389/fimmu.2021.832980. eCollection 2021.
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Immunoregulatory Effects of Myeloid-Derived Suppressor Cell Exosomes in Mouse Model of Autoimmune Alopecia Areata.骨髓来源的抑制性细胞外泌体在自身免疫性斑秃小鼠模型中的免疫调节作用。
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SOCS3 treatment prevents the development of alopecia areata by inhibiting CD8+ T cell-mediated autoimmune destruction.细胞因子信号转导抑制因子3（SOCS3）治疗通过抑制CD8 + T细胞介导的自身免疫性破坏来预防斑秃的发生。
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Alopecia areata: a tissue specific autoimmune disease of the hair follicle.斑秃：一种毛囊的组织特异性自身免疫性疾病。
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Suppressor cell decrease in alopecia areata.斑秃中抑制细胞减少。
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Resistance to alopecia areata in C3H/HeJ mice is associated with increased expression of regulatory cytokines and a failure to recruit CD4+ and CD8+ cells.C3H/HeJ小鼠对斑秃的抗性与调节性细胞因子表达增加以及无法募集CD4+和CD8+细胞有关。
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[Alopecia areata in animal models--new insights into pathogenesis and treatment of a T cell-mediated autoimmune disorder].[动物模型中的斑秃——对一种T细胞介导的自身免疫性疾病发病机制及治疗的新见解]
J Dtsch Dermatol Ges. 2004 Apr;2(4):260-73. doi: 10.1046/j.1610-0387.2003.03553.x-i1.
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Transient CD44 variant isoform expression and reduction in CD4(+)/CD25(+) regulatory T cells in C3H/HeJ mice with alopecia areata.斑秃C3H/HeJ小鼠中CD44可变剪接异构体的瞬时表达及CD4(+)/CD25(+)调节性T细胞减少
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Vitamin D and alopecia areata: possible roles in pathogenesis and potential implications for therapy.维生素D与斑秃：在发病机制中的可能作用及对治疗的潜在意义。
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Melanocyte-associated T cell epitopes can function as autoantigens for transfer of alopecia areata to human scalp explants on Prkdc(scid) mice.黑素细胞相关的T细胞表位可作为自身抗原，将斑秃转移至Prkdc(scid)小鼠的人头皮外植体上。
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