ALLERGEN-SPECIFIC AND BACTERIAL ANTIGEN-SPECIFIC T-CELL CLONES ESTABLISHED FROM ATOPIC DONORS SHOW A DIFFERENT PROFILE OF CYTOKINE PRODUCTION
ALLERGEN-SPECIFIC AND BACTERIAL ANTIGEN-SPECIFIC T-CELL CLONES ESTABLISHED FROM ATOPIC DONORS SHOW A DIFFERENT PROFILE OF CYTOKINE PRODUCTION
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DOI：
10.1073/pnas.88.10.4538
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发表时间：
1991-05-01
影响因子：
11.1
通讯作者：
ROMAGNANI, S
中科院分区：
文献类型：
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作者：
PARRONCHI, P;MACCHIA, D;ROMAGNANI, S
我们从两名特应性个体的外周血中建立了大量针对屋尘螨和黑麦草I组草花粉过敏原（共61个）以及破伤风类毒素和结核菌素纯蛋白衍生物细菌抗原（共38个）的T细胞克隆（TCC），然后分析了它们产生白细胞介素4（IL - 4）、IL - 5和干扰素 - γ（IFN - γ）的能力。在用佛波醇12 - 肉豆蔻酸酯13 - 乙酸酯加抗CD3抗体刺激后，大多数针对细菌成分的TCC能够产生IL - 4和IFN - γ，而大多数屋尘螨和黑麦草I组特异性TCC产生IL - 4，但不产生或仅产生有限的IFN - γ。此外，过敏原特异性TCC释放的IL - 4和IFN - γ的平均量分别显著高于和低于细菌成分特异性TCC产生的平均量。在相同的实验条件下，几乎所有过敏原特异性TCC，但只有三分之一的受测细菌成分特异性TCC在上清液中表达IL - 5 RNA并分泌IL - 5。还评估了18个TCC（9个针对过敏原，9个针对细菌成分）在受到特异性抗原刺激时诱导自体B细胞合成IgE的能力。在这些实验条件下，所有过敏原特异性TCC，但只有三分之一产生IL - 4但不产生或几乎不产生IFN - γ的细菌成分特异性TCC诱导了可检测量的IgE合成。特应性个体中大多数过敏原特异性辅助性T细胞能够产生大量IL - 4（和IL - 5）但不产生IFN - γ这一证明，可能解释了为什么过敏原会诱导IgE抗体的产生并使嗜酸性粒细胞增加。
We have established a large panel of T-cell clones (TCCs) specific for Dermatophagoides pteronyssinus and Lolium perenne group I grass pollen allergens (total, 61) and for tetanus toxoid and protein purified derivative bacterial antigens (total, 38) from the peripheral blood of two atopic individuals and then analyzed their ability to produce interleukin 4 (IL-4), IL-5, and interferon-gamma (IFN-gamma). Upon stimulation with phorbol 12-myristate 13-acetate plus anti-CD3 antibody, the great majority of TCCs specific for bacterial components was able to produce both IL-4 and IFN-gamma, whereas most D. pteronyssinus- and L. perenne group I-specific TCCs produced IL-4, but no, or limited, IFN-gamma. Moreover, the mean amounts of IL-4 and IFN-gamma released by allergen-specific TCCs were significantly higher and lower, respectively, than the mean amounts produced by TCCs specific for bacterial components. Under the same experimental conditions, virtually all allergen-specific TCCs, but only one-third of tested TCCs specific for bacterial components, expressed IL-5 RNA and secreted IL-5 in their supernatants. Eighteen TCCs (nine specific for allergens and nine specific for bacterial components) were also assessed for their ability to induce IgE synthesis by autologous B cells in response to stimulation with the specific antigen. Under these experimental conditions, all allergen-specific TCCs, but only one-third of TCCs specific for bacterial components that produced IL-4 but no, or little, IFN-gamma induced the synthesis of detectable amounts of IgE. The demonstration that most allergen-specific helper T cells in atopic individuals are able to produce high amounts of IL-4 (and IL-5), but no IFN-gamma, may explain why allergens induce production of IgE antibodies and increase eosinophils.