Miller K, Hudspith B N, Meredith C
Immunotoxicology Department, British Industrial Biological Research Association, Carshalton, Surrey, UK.
Environ Health Perspect. 1992 Jul;97:85-9. doi: 10.1289/ehp.929785.
We have attempted to address the requirements necessary for alveolar macrophage accessory cell function. We have also examined the in vitro and in vivo factors that must be taken into account when interpreting results from experimental studies. Differences in phenotypic expression by rat alveolar pleural and peritoneal macrophages are noted, as well as the differing expression of major histocompatibility complex (MHC) class II molecules. Furthermore, alveolar macrophages, harvested from rat lung, do not express the interleukin (IL)-1 cytokines, and lipopolysaccharide (LPS) treatment of quiescent cells (after 24-hr in vitro culture) induces low levels of expression of IL-1 alpha and IL-1 beta. Short-term inhalation of refractory ceramic fibers, however, results in markedly increased IL-1 beta expression after stimulation with LPS. We suggest that, in vivo, IL-1 beta may be involved in the initial recruitment and activation of inflammatory cells rather than in induction of immune responses. We also postulate, based on recent published evidence, that alveolar macrophages activate the dendritic cells within the respiratory epithelium. Thus alveolar macrophages would release cytokines critical for the activation of dendritic cells during the afferent limb of the immune response, and they would respond to products of sensitized T-cells such as interferon-gamma and IL-4 to interact with T-helper cells in an antigen-specific MHC-restricted manner during the efferent limb of the response.
我们已尝试满足肺泡巨噬细胞辅助细胞功能所需的条件。我们还研究了在解释实验研究结果时必须考虑的体外和体内因素。注意到大鼠肺泡、胸膜和腹膜巨噬细胞在表型表达上存在差异,以及主要组织相容性复合体(MHC)II类分子的表达差异。此外,从大鼠肺中收获的肺泡巨噬细胞不表达白细胞介素(IL)-1细胞因子,静止细胞(体外培养24小时后)经脂多糖(LPS)处理会诱导IL-1α和IL-1β的低水平表达。然而,短期吸入难熔陶瓷纤维会导致在用LPS刺激后IL-1β表达显著增加。我们认为,在体内,IL-1β可能参与炎症细胞的初始募集和激活,而不是免疫反应的诱导。我们还根据最近发表的证据推测,肺泡巨噬细胞激活呼吸道上皮内的树突状细胞。因此,肺泡巨噬细胞在免疫反应的传入阶段会释放对树突状细胞激活至关重要的细胞因子,并且它们会在反应的传出阶段以抗原特异性MHC限制的方式对致敏T细胞的产物如干扰素-γ和IL-4作出反应,以与辅助性T细胞相互作用。