Hancock W W, Muller W A, Cotran R S
J Immunol. 1987 Jan 1;138(1):185-91.
Expression of receptors for IL 2 was believed initially to be restricted to T cells after their activation by IL 1 and antigen. However, recently IL 2 receptors (IL 2R) were demonstrated on activated B cells by using an anti-IL 2R monoclonal antibody (anti-Tac). In this study, we examined the capacity of cultured human alveolar macrophages, blood monocytes, and myelomonocytic (HL-60) or monoblast (U937) cell lines to bind three different anti-IL 2R monoclonal antibodies before or after stimulation with the monocyte-activating agents IFN-gamma, LPS, phorbol ester, or lymphokine-containing conditioned medium. For each of the four cell populations examined, resting unstimulated cells bound little or no anti-IL 2R antibody, as shown independently by quantitative cell binding assay and by immunoperoxidase labeling. By contrast, incubation with recombinant IFN-gamma, conditioned medium, or to a lesser extent, native or recombinant IL 2 itself, resulted in a significant enhancement of anti-IL 2 receptor monoclonal antibody binding by all four populations, whereas LPS, PMA, or IL 1 had no effect. In addition, membrane binding of anti-Tac antibody, similar to that seen after stimulation of normal lung macrophages with IFN-gamma, was detected by using macrophages obtained by bronchoalveolar lavage of five patients with active pulmonary sarcoidosis. These findings are consistent with the expression of a functional IL 2R on activated cells of the monocyte lineage, since anti-Tac binding to IFN-gamma-treated HL-60 cells was inhibited by addition of excess IL-2; specific binding of anti-IL 2 monoclonal antibodies was detected in the presence of exogenous IL 2; and a 50 to 55 kD molecule was immunoprecipitated from both activated lung macrophages and T lymphoblasts by using anti-Tac antibody. We conclude that human mononuclear phagocytes can be induced by lymphokines to express IL 2R, and that such IL 2R+ macrophages can be detected in vivo during inflammation.
白细胞介素2（IL 2）受体的表达最初被认为仅限于T细胞在被IL 1和抗原激活之后。然而，最近通过使用抗IL 2受体单克隆抗体（抗Tac）在活化的B细胞上证实了IL 2受体（IL 2R）的存在。在本研究中，我们检测了培养的人肺泡巨噬细胞、血液单核细胞以及髓单核细胞（HL - 60）或单核母细胞（U937）细胞系在被单核细胞激活剂干扰素-γ（IFN -γ）、脂多糖（LPS）、佛波酯或含淋巴因子的条件培养基刺激之前或之后结合三种不同抗IL 2R单克隆抗体的能力。对于所检测的四种细胞群体中的每一种，通过定量细胞结合试验和免疫过氧化物酶标记独立显示，静息未受刺激的细胞结合很少或不结合抗IL 2R抗体。相比之下，用重组IFN -γ、条件培养基孵育，或者在较小程度上用天然或重组IL 2本身孵育，导致所有四种细胞群体对抗IL 2受体单克隆抗体的结合显著增强，而LPS、佛波酯（PMA）或IL l则没有作用。此外，通过使用从五名活动性肺结节病患者的支气管肺泡灌洗获得的巨噬细胞，检测到抗Tac抗体的膜结合，类似于用IFN -γ刺激正常肺巨噬细胞后所见。这些发现与单核细胞系活化细胞上功能性IL 2R的表达一致，因为向IFN -γ处理的HL - 60细胞中加入过量IL - 2可抑制抗Tac的结合；在外源性IL 2存在的情况下检测到抗IL 2单克隆抗体的特异性结合；并且使用抗Tac抗体从活化的肺巨噬细胞和T淋巴母细胞中免疫沉淀出一种50至55kD的分子。我们得出结论，人单核吞噬细胞可被淋巴因子诱导表达IL 2R，并且在炎症期间可在体内检测到这种IL 2R +巨噬细胞。
