Cooper K D, Kang K, Hanifin J M
Diagn Immunol. 1983;1(3):211-5.
Atopic dermatitis (AD) patients exhibit multiple immune abnormalities, including T-cell defects that may be partially correctable by the administration of thymic hormones. Our investigations confirmed that peripheral blood mononuclear leukocytes obtained from patients with AD spontaneously synthesized markedly elevated amounts of IgE in vitro. The thymic hormone thymopoietin pentapeptide (TP-5) greatly inhibited this synthesis. An antihuman pan-T cell monoclonal antibody (Lyt3) was used to separate T-cell marker-positive (T+) T cells from marker-negative (T-) B-enriched cells. TP-5 pretreatment of T+ cells resulted in significant reduction of in vitro IgE synthesis by recombined T+ and T- cells, whereas pretreatment of T- B-enriched cells resulted in a nonsignificant reduction in in vitro IgE synthesis. Thus, although pretreatment of both subsets resulted in some degree of reduction, TP-5-induced inhibition of in vitro IgE synthesis was primarily mediated via T cells. The majority of patients' untreated T+ and T4+ cells showed enhanced IgE synthesis, but only one patient's T8+ cells were capable of suppressing IgE synthesis. Thus TP-5 may either induce suppressor T-cell activity or reduce helper T-cell activity. A six-week double-blind clinical trial of TP-5 produced evidence of clinical improvement and alterations of abnormalities of OKT8+ cells, although no significant effects on serum IgE were seen.
特应性皮炎(AD)患者表现出多种免疫异常,包括T细胞缺陷,而给予胸腺激素可能会部分纠正这些缺陷。我们的研究证实,从AD患者获得的外周血单个核白细胞在体外可自发合成显著升高量的IgE。胸腺激素胸腺生成素五肽(TP-5)可极大地抑制这种合成。使用抗人全T细胞单克隆抗体(Lyt3)从标记阴性(T-)富含B细胞中分离出T细胞标记阳性(T+)的T细胞。对T+细胞进行TP-5预处理可使重组的T+和T-细胞在体外合成的IgE显著减少,而对富含T- B细胞进行预处理则使体外IgE合成减少不显著。因此,尽管对两个亚群进行预处理都导致了一定程度的减少,但TP-5诱导的体外IgE合成抑制主要是通过T细胞介导的。大多数患者未经处理的T+和T4+细胞显示出增强的IgE合成,但只有一名患者的T8+细胞能够抑制IgE合成。因此,TP-5可能要么诱导抑制性T细胞活性,要么降低辅助性T细胞活性。一项为期六周的TP-5双盲临床试验产生了临床改善以及OKT8+细胞异常改变的证据,尽管未观察到对血清IgE有显著影响。