Ina Y, Takada K, Yamamoto M, Morishita M, Miyachi A
Second Department of Internal Medicine, Nagoya City University Medical School, Japan.
Chest. 1990 Oct;98(4):911-6. doi: 10.1378/chest.98.4.911.
Antigen-presenting capacity by monocytes and AMs was determined in 13 patients with sarcoidosis and nine healthy control subjects, using PPD as the antigen. The patients and healthy control subjects all had positive PPD skin tests. Monocytes from both the control subjects and the patients with sarcoidosis exhibited antigen-presenting capacity to autologous peripheral T-lymphocytes, without any significant difference between the two groups. The AMs from patients, but not control subjects, demonstrated antigen-presenting capacity to autologous peripheral T-lymphocytes. Antigen-presenting capacity by monocytes and AMs to lung T-lymphocytes was lower than to peripheral T-lymphocytes, but not significantly. Antigen-presenting capacity was not significantly different between patients with sarcoidosis who had positive and negative PPD skin tests. The mechanism of enhanced antigen-presenting capacity by AMs in sarcoidosis is uncertain at present, but no significant difference was observed in DR antigen expression on AMs between controls and patients with sarcoidosis, and the addition of exogenous IL-1 or IFN-gamma did not induce antigen-presenting capacity by AMs in controls, suggesting that neither increased DR antigen expression on AMs nor increased release of IL-1 or IFN-gamma from AMs is responsible. Thus, these results suggest that T-lymphocyte activation in sarcoidosis may in part be attributable to an enhanced antigen-presenting capacity by AMs.
以结核菌素纯蛋白衍生物（PPD）作为抗原，在13例结节病患者和9名健康对照者中测定了单核细胞和肺泡巨噬细胞（AMs）的抗原呈递能力。患者和健康对照者的PPD皮肤试验均呈阳性。对照者和结节病患者的单核细胞均表现出对自身外周T淋巴细胞的抗原呈递能力，两组之间无显著差异。患者的AMs表现出对自身外周T淋巴细胞的抗原呈递能力，而对照者的AMs则未表现出这种能力。单核细胞和AMs对肺T淋巴细胞的抗原呈递能力低于对外周T淋巴细胞的抗原呈递能力，但差异不显著。PPD皮肤试验阳性和阴性的结节病患者之间的抗原呈递能力无显著差异。目前尚不清楚结节病中AMs抗原呈递能力增强的机制，但对照者和结节病患者的AMs上DR抗原表达未观察到显著差异，并且添加外源性白细胞介素-1（IL-1）或γ干扰素（IFN-γ）并未诱导对照者的AMs产生抗原呈递能力，这表明AMs上DR抗原表达增加以及AMs释放IL-1或IFN-γ增加均不是其原因。因此，这些结果表明结节病中T淋巴细胞活化可能部分归因于AMs抗原呈递能力增强。
