Human alveolar macrophage regulation of lymphocyte proliferation.
Human alveolar macrophage regulation of lymphocyte proliferation.
复制标题
人肺泡巨噬细胞对淋巴细胞增殖的调节。
DOI：
10.1164/arrd.1986.133.6.1091
复制
发表时间：
1986
期刊：
影响因子：
--
通讯作者：
RobertsJr,NJ
中科院分区：
文献类型：
--
作者：
Ettensohn,DB;Lalor,PA;RobertsJr,NJ
通过支气管肺泡灌洗获得的人肺泡巨噬细胞与自体外周血来源的巨噬细胞相比具有不同的辅助细胞特征，以支持淋巴细胞增殖反应。为了进一步研究这些差异，我们进行了混合实验，其中共培养了不同数量的 2 种巨噬细胞，并分析了丝裂原（植物血凝素；PHA）和抗原（链激酶-链球菌酶；SK-SD）刺激纯化自体淋巴细胞增殖的支持。当使用次优浓度的 PHA 时，肺泡巨噬细胞促进更大的淋巴细胞增殖，与与外周血来源的巨噬细胞共培养时增加的数量成比例。相比之下，当使用最佳浓度的 PHA 或抗原 SK-SD 时，即使是少量的肺泡巨噬细胞也能抑制由外周血来源的巨噬细胞支持的淋巴细胞增殖。数据表明，肺泡巨噬细胞对最佳有丝分裂原刺激或抗原刺激的淋巴细胞反应的支持减弱是由于细胞的主动抑制，而不是由于辅助细胞功能的缺陷或缺陷。因此，肺泡巨噬细胞对淋巴细胞增殖具有调节作用，这取决于促有丝分裂刺激的类型和浓度。这种调节可能与体内肺泡巨噬细胞的功能有关，提供适当的反应，同时限制肺部炎症。
Human alveolar macrophages obtained by bronchoalveolar lavage have different accessory cell characteristics than do autologous, peripheral-blood-derived macrophages for the support of lymphocyte proliferative responses. To further investigate these differences, we performed mixing experiments in which variable numbers of the 2 macrophages were cocultured and assayed for support of mitogen-(phytohemagglutinin; PHA) and antigen- (streptokinase-streptodornase; SK-SD) stimulated proliferation of purified autologous lymphocytes. Alveolar macrophages promoted greater lymphocyte proliferation, in proportion to their added number in coculture with peripheral-blood-derived macrophages, when using a suboptimal concentration of PHA. In contrast, even small numbers of alveolar macrophages suppressed lymphocyte proliferation supported by peripheral-blood-derived macrophages when using the optimal concentration of PHA or the antigen SK-SD. The data indicated that diminished support exhibited by alveolar macrophages for optimal mitogen-stimulated or antigen-stimulated lymphocyte responses was due to active suppression by the cells, rather than to deficient or defective accessory cell function. Thus, alveolar macrophages have regulatory effects on lymphocyte proliferation that are dependent on type and concentration of mitogenic stimulation. Such regulation may relate to alveolar macrophage functionin vivo,providing appropriate response yet limiting inflammation in the lung.