哮喘严重程度：CD25+、CD30+、NF-κB和凋亡标记物的作用
2009/09/16
目的：本实验在轻症间歇性哮喘患者（MA）、严重持续性哮喘患者（SA）和健康志愿者（HV）中研究调节性T细胞CD4+CD25+ (Treg) 和活化的CD4+CD30+细胞在哮喘致病过程中的作用，以及它们与凋亡和NF-κB之间的关系。
方法：收集哮喘患者恶化期的外周血淋巴细胞（PBL），采用Dynal磁珠分离CD4+细胞。采用细胞免疫化学技术对全PBL中的NF-κB、Bax和 Bcl-2进行免疫染色，同时对CD4+细胞中的CD25+和CD30+细胞进行免疫染色。
结果：MA患者外周血淋巴细胞中的Treg细胞水平较HV和SA患者高（P<0.05），而SA和MA患者中CD30+T细胞的表达高于HV人群，虽然SA与MA患者之间未见显著性差异（P>0.05）。从MA到SA患者，NF-κB、Bcl-2和Bcl-2/Bax水平增加，而Bax降低（P <0.05）。在SA与MA患者中，NF-κB水平与Bcl-2/Bax 比和CD4+CD30+细胞直接相关，而CD4+CD30+细胞与Bcl-2/Bax 比呈负相关。
结论：MA患者哮喘恶化期间，未受调节的Treg细胞能将炎症反应恢复至正常水平。而在SA患者中，Treg细胞的表达受到广泛抑制，导致对免疫反应的抑制效应丧失。CD4+CD30+细胞与哮喘的致病过程有关，但与哮喘严重程度无关。在SA患者中，NF-κB可能是重要的炎症因子，患者PBL的大幅凋亡丧失、Treg细胞水平降低以及较高的CD30+水平能诱导NF-κB，NF-κB反过来阻断了CD30自身诱导的促凋亡作用。
（苏楠 审校）
Abdulamir AS, Kadhim HS, Hafidh RR, et al.
J Investig Allergol Clin Immunol. 2009;19(3):218-24.
Severity of asthma: the role of CD25+, CD30+, NF-kappaB, and apoptotic markers.
Abdulamir AS, Kadhim HS, Hafidh RR, Ali MA, Faik I, Abubakar F, Abbas KA.
Microbiology Research Department, University Putra Malaysia, Serdang, Malaysia. ahmsah73@yahoo.com
OBJECTIVES: We studied the role of the regulatory T cells CD4+CD25+ (Treg) and activated CD4+CD30+ cells in the pathogenesis of asthma and their association with apoptosis and NF-kappaB in patients with mild intermittent asthma (MA), severe persistent asthma (SA), and healthy volunteers (HV).
METHODS: Peripheral blood lymphocytes (PBL) were extracted from asthmatic patients during exacerbations, and CD4+ cells were separated using Dynal beads. Immunostaining of whole PBL for NF-kappaB, Bax, and Bcl-2, and immunostaining of CD4+ cells for CD25+ and CD30+ cells were performed using immunocytochemistry.
RESULTS: Treg cells were expressed at higher levels in MA than in HV and SA (P < .05), while CD30+ T cells were expressed at higher levels in both SA and MA than in HV (P < .05), although there was no remarkable difference between SA and MA (P>.05). Levels of NF-kappaB, Bcl-2, and Bcl-2/Bax increased, whereas those of Bax decreased, progressively, from MA to SA (P < .05). NF-kappaB levels correlated directly with the Bcl-2/Bax ratio and with CD4+CD30+ cells in SA and MA, whereas CD4+CD30+ cells correlated inversely with the Bcl-2/Bax ratio.
CONCLUSIONS: Unregulated Treg cells probably return inflammatory responses to normal values during exacerbations in MA; however, expression of Treg cells was extensively diminished in SA, leading to probable loss of suppressive control over underlying immune reactions. CD4+CD30+ cells were associated with the pathogenesis of asthma but not with severity. NF-kappaB seems to be the central inflammatory factor in SA, with a remarkable loss of PBL apoptosis, diminished Treg levels, and high CD30+ cell levels that probably induce NF-kappaB, which in turn blocks the proapoptotic potential of CD30 induction itself.
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