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由于急促的气流通过易受刺激的、狭窄和增厚的气道而产生哮喘的声音。这种支气管炎症导致的变化,主要是由TH2引起。TH2分泌白介素(IL)促进过敏性炎症的产生、刺激B细胞产生IgE等其它抗体。而TH1可分泌IFN-γ和IL-2,后者可通过激活巨噬细胞和细胞素性T细胞来杀伤病毒或其他细胞。对于不同的免疫刺激或细胞因子,这两种TH可增高并形成免疫调控环路,即TH1分泌的细胞因子可抑制TH2细胞的活性,反之亦然。有足够的证据表明,这种调控环路的破坏可能是引起哮喘的关键所在。当排除IFN-γ的限制性影响后,TH2可增强气道的炎症。
The sound of asthma is caused by the rapid flow of air through irritable, stenotic and thickened airways. This bronchitis-induced change is mainly caused by TH2. TH2 secretion of interleukin (IL) promote the production of allergic inflammation, stimulate B cells to produce IgE and other antibodies. While TH1 secretes IFN-γ and IL-2, the latter can kill viruses or other cells by activating macrophages and cytokine T cells. For different immune stimuli or cytokines, both THs can increase and form an immune regulatory loop, that is, TH1-secreted cytokines can inhibit TH2 cell activity and vice versa. There is sufficient evidence that the destruction of this regulatory loop may be the key to asthma. TH2 enhances airway inflammation when excluding the limiting effects of IFN-γ.