Furuie H, Yamasaki H, Suga M, Ando M
First Department of Internal Medicine, Kumamoto University School of Medicine, Japan.
Eur Respir J. 1997 Apr;10(4):787-94.
Alveolar macrophages (AMs) are considered to play a central role in the pathogenesis of idiopathic pulmonary fibrosis (IPF). Recent studies have revealed a predominance of the type-2 T-helper (Th2) cytokine pattern of inflammatory response in the pulmonary interstitium in IPF. The aim of the present study was to determine whether or not the altered accessory cell function of AMs could account for the Th2 pattern of chronic inflammation in IPF. The levels of various cytokines were measured in the supernatants of soluble anti-CD3 monoclonal antibody (MoAb)-stimulated T-cells, co-cultured with autologous AMs, by enzyme-linked immunosorbent assay (ELISA). Cells from six patients with IPF and from nine normal volunteers (five nonsmokers and four smokers) were examined. The inhibitory effect of interleukin (IL)-10 on the accessory cell function of AMs and the expression of CD80 and CD86 on AMs were also investigated. IL-4 and IL-5 levels were significantly higher in the co-cultures from patients with IPF than in those from normal volunteers. IL-2, interferon-gamma (IFN-gamma), and IL-10 production in these co-cultures did not differ. IL-10 suppressed T-cell proliferation in co-cultures with AMs from healthy volunteers (smokers and nonsmokers), but not with AMs from patients with IPF. Expression of CD80 and CD86 on AMs from these groups did not differ. Thus, the altered accessory cell function of alveolar macrophages from patients with idiopathic pulmonary fibrosis may possibly relate to the pattern of type-2 T-helper cytokine production in response to inflammation.
肺泡巨噬细胞（AMs）被认为在特发性肺纤维化（IPF）的发病机制中起核心作用。最近的研究表明，IPF患者肺间质中炎症反应以2型辅助性T细胞（Th2）细胞因子模式为主。本研究的目的是确定AMs辅助细胞功能的改变是否可以解释IPF中慢性炎症的Th2模式。通过酶联免疫吸附测定（ELISA），在与自体AMs共培养的可溶性抗CD3单克隆抗体（MoAb）刺激的T细胞上清液中测量各种细胞因子的水平。检测了6例IPF患者和9名正常志愿者（5名非吸烟者和4名吸烟者）的细胞。还研究了白细胞介素（IL）-10对AMs辅助细胞功能的抑制作用以及AMs上CD80和CD86的表达。IPF患者共培养物中的IL-4和IL-5水平显著高于正常志愿者。这些共培养物中IL-2、干扰素-γ（IFN-γ）和IL-10的产生没有差异。IL-10抑制了与健康志愿者（吸烟者和非吸烟者）的AMs共培养中的T细胞增殖，但对IPF患者的AMs没有抑制作用。这些组中AMs上CD80和CD86的表达没有差异。因此，特发性肺纤维化患者肺泡巨噬细胞辅助细胞功能的改变可能与炎症反应中2型辅助性T细胞细胞因子产生模式有关。
