Anderson G P, Coyle A J
Research Department CIBA, Basel, Switzerland.
Trends Pharmacol Sci. 1994 Sep;15(9):324-32. doi: 10.1016/0165-6147(94)90027-2.
Recently, considerable progress has been made in understanding the molecular basis by which cytokines released from CD4+ helper T cells contribute to allergic disease. A subset of CD4+ helper T cells, termed TH2 cells, produce interleukin 4 (IL-4) and IL-5, but not interferon gamma. IL-4 has a critical role in causing B-cell immunoglobulin-isotype switch leading to IgE synthesis, and IL-5 governs eosinophilic inflammation of airway tissue. Studies on the mechanisms whereby TH2 cells, and non-T cells such as metachromatic cells, produce a highly restricted panel of cytokines has revealed molecular mechanisms that may affect our views on the induction and treatment of asthma, and these are discussed in this review by Gary Anderson and Anthony Coyle. TH2 cytokine biology may enable pharmacologists to design better, and perhaps even preventative, therapies for the treatment of asthma and allergy. Surprisingly IL-4, rather than IL-5, is emerging as a critical drug target owing to its central role in the regulation of CD4+ helper T cell phenotype commitment.
最近,在理解CD4 +辅助性T细胞释放的细胞因子导致过敏性疾病的分子基础方面取得了相当大的进展。CD4 +辅助性T细胞的一个亚群,称为TH2细胞,产生白细胞介素4(IL-4)和IL-5,但不产生干扰素γ。IL-4在导致B细胞免疫球蛋白同种型转换从而导致IgE合成方面起关键作用,而IL-5则控制气道组织的嗜酸性粒细胞炎症。关于TH2细胞以及诸如异染细胞等非T细胞产生一组高度受限的细胞因子的机制的研究揭示了可能影响我们对哮喘诱导和治疗观点的分子机制,加里·安德森和安东尼·科伊尔在本综述中对此进行了讨论。TH2细胞因子生物学可能使药理学家能够设计出更好的,甚至可能是预防性的治疗哮喘和过敏的疗法。令人惊讶的是,由于IL-4在调节CD4 +辅助性T细胞表型决定中的核心作用,它正成为一个关键的药物靶点,而不是IL-5。