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斑秃DEBR模型中,体内CD4 + T细胞耗竭后毛发生长的部分恢复。

Partial restoration of hair growth in the DEBR model for Alopecia areata after in vivo depletion of CD4+ T cells.

作者信息

McElwee K J, Spiers E M, Oliver R F

机构信息

Department of Biological Sciences, University of Dundee, Dundee, DD1 4HN, U.K.

出版信息

Br J Dermatol. 1999 Mar;140(3):432-7. doi: 10.1046/j.1365-2133.1999.02705.x.

DOI:10.1046/j.1365-2133.1999.02705.x
PMID:10233262
Abstract

Alopecia areata (AA) is widely believed to be an autoimmune disease. Hair loss is associated with a peri- and intrafollicular inflammatory infiltrate of anagen hair follicles primarily composed of CD4 + and CD8 + cells. A previous investigation involved in vivo depletion of CD8 + cells in the DEBR rat model to examine the cells' potential pathogenic activity in AA. The rat model is used here in a comparable study of CD4 + cell pathogenic activity. Eight AA affected DEBR rats were given intraperitoneal injections of a CD4 + cell depleting OX-35/OX-38 monoclonal antibody (MoAb) cocktail over a 15-day therapy course. A further eight AA-affected rats comprised a control group and were injected with equivalent volumes of an irrelevant MoAb, OX-21. Changes in both CD4 + and CD8 + peripheral blood cell populations were analysed by flow cytometry, and macrophotography was used to record any changes in hair growth. Of the eight CD4 + cell-depleted rats six responded with hair growth. The rats revealed significant hair growth within 23 days of treatment initiation. With rapid replacement of the CD4 + cell population the newly generated pelage hair was eventually lost. Two control rats also showed limited hair growth within the 112-day study period. In vivo depletion of CD4 + cells partially restores hair growth in AA affected rats. The response suggests that CD4 + cells may be actively involved in the pathogenesis of AA. Further research may elucidate whether CD4 + cells have a direct effect on hair follicles or exert their influence through their classic T helper cell supporting role for CD8 + cells.

摘要

斑秃(AA)被广泛认为是一种自身免疫性疾病。脱发与生长期毛囊周围和毛囊内主要由CD4 +和CD8 +细胞组成的炎性浸润有关。先前的一项研究在DEBR大鼠模型中对CD8 +细胞进行体内清除,以检查这些细胞在斑秃中的潜在致病活性。在此,该大鼠模型用于一项关于CD4 +细胞致病活性的可比研究。八只患有斑秃的DEBR大鼠在为期15天的治疗过程中腹腔注射一种清除CD4 +细胞的OX-35/OX-38单克隆抗体(MoAb)鸡尾酒。另外八只患有斑秃的大鼠组成对照组,注射等量的无关单克隆抗体OX-21。通过流式细胞术分析CD4 +和CD8 +外周血细胞群的变化,并使用宏观摄影记录毛发生长的任何变化。在八只CD4 +细胞被清除的大鼠中,有六只出现毛发生长。这些大鼠在开始治疗后的23天内显示出明显的毛发生长。随着CD4 +细胞群的快速恢复,新长出的被毛最终脱落。两只对照大鼠在112天的研究期内也显示出有限的毛发生长。在体内清除CD4 +细胞可部分恢复患有斑秃的大鼠的毛发生长。这一反应表明CD4 +细胞可能积极参与斑秃的发病机制。进一步的研究可能会阐明CD4 +细胞是否对毛囊有直接作用,或者是否通过其对CD8 +细胞的经典辅助性T细胞支持作用发挥影响。

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Partial restoration of hair growth in the DEBR model for Alopecia areata after in vivo depletion of CD4+ T cells.斑秃DEBR模型中,体内CD4 + T细胞耗竭后毛发生长的部分恢复。
Br J Dermatol. 1999 Mar;140(3):432-7. doi: 10.1046/j.1365-2133.1999.02705.x.
2
In vivo depletion of CD8+ T cells restores hair growth in the DEBR model for alopecia areata.在斑秃的DEBR模型中,体内清除CD8 + T细胞可恢复头发生长。
Br J Dermatol. 1996 Aug;135(2):211-7.
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Immunohistological study of the development of the cellular infiltrate in the pelage follicles of the DEBR model for alopecia areata.斑秃DEBR模型毛囊中细胞浸润发展的免疫组织学研究。
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Alopecia areata in C3H/HeJ mice involves leukocyte-mediated root sheath disruption in advance of overt hair loss.C3H/HeJ小鼠的斑秃在明显脱发之前涉及白细胞介导的毛囊外根鞘破坏。
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The role of lymphocytes in the development and treatment of alopecia areata.淋巴细胞在斑秃发病及治疗中的作用。
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The DEBR rat, alopecia areata and autoantibodies to the hair follicle.DEBR大鼠、斑秃与毛囊自身抗体。
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Expression of vascular endothelial growth factor, apoptosis inhibitors (survivin and p16) and CCL27 in alopecia areata before and after diphencyprone treatment: an immunohistochemical study.二苯环丙烯酮治疗前后斑秃中血管内皮生长因子、凋亡抑制因子(生存素和p16)及CCL27的表达:一项免疫组织化学研究
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Mediation of alopecia areata by cooperation between CD4+ and CD8+ T lymphocytes: transfer to human scalp explants on Prkdc(scid) mice.CD4+和CD8+ T淋巴细胞之间的合作介导斑秃:移植到Prkdc(scid)小鼠的人头皮外植体上。
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Substance P as an immunomodulatory neuropeptide in a mouse model for autoimmune hair loss (alopecia areata).在自身免疫性脱发(斑秃)小鼠模型中,P物质作为一种免疫调节性神经肽。
J Invest Dermatol. 2007 Jun;127(6):1489-97. doi: 10.1038/sj.jid.5700704. Epub 2007 Feb 1.

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