McDonald C F, Hutchinson P, Atkins R C
Department of Thoracic Medicine, Repatriation General Hospital, Heidelberg, Victoria, Australia.
Clin Exp Immunol. 1993 Jan;91(1):126-30. doi: 10.1111/j.1365-2249.1993.tb03366.x.
We have previously described alterations in pulmonary alveolar macrophage (PAM) function in patients with lung cancer when compared with control subjects. This study examined PAM from five patients with lung cancer, seven normal volunteers and nine control patients, to assess whether any differences in surface phenotypic markers were present in lung cancer versus non-cancer subjects, and what changes might be induced with interferon-gamma (IFN-gamma) stimulation. After 3 days' culture with or without IFN-gamma no differences were seen in the percentages of cells staining positively in each group for HLA class I, class II and ICAM-1 (CD54) antigens. However, in 13 out of 14 control subjects, and only one out of the five cancer subjects, dual PAM populations were identified. The second PAM population (PAM-2) was larger and demonstrated a higher expression of class I and ICAM-1 antigens. Unlike the unfractionated PAM population, PAM-2 consistently responded to IFN-gamma stimulation with an increase in both class I (90 +/- 25%) and ICAM-1 (45 +/- 10%) antigens, while there was no change in class II antigen expression. In three subjects PAM-2 was found to induce a significantly greater mitogen response than the rest of the PAM population. If confirmed in a larger group of patients, the absence of PAM-2 in the majority of patients with lung cancer may underlie the functional PAM defects observed in these patients.
我们之前曾描述过,与对照受试者相比,肺癌患者肺泡巨噬细胞(PAM)功能存在改变。本研究检测了5例肺癌患者、7名正常志愿者和9例对照患者的PAM,以评估肺癌患者与非癌症患者在表面表型标志物方面是否存在差异,以及γ干扰素(IFN-γ)刺激可能会引起哪些变化。在有或无IFN-γ的情况下培养3天后,每组中HLA I类、II类和细胞间黏附分子-1(CD54)抗原呈阳性染色的细胞百分比未见差异。然而,在14名对照受试者中有13名,而5名癌症受试者中只有1名,鉴定出了双重PAM群体。第二个PAM群体(PAM-2)更大,且I类和ICAM-1抗原表达更高。与未分离的PAM群体不同,PAM-2对IFN-γ刺激始终有反应,I类抗原(90±25%)和ICAM-1抗原(45±10%)均增加,而II类抗原表达无变化。在3名受试者中,发现PAM-2诱导的丝裂原反应明显大于其余PAM群体。如果在更大规模的患者群体中得到证实,大多数肺癌患者中缺乏PAM-2可能是这些患者中观察到的功能性PAM缺陷的基础。