Suriki H, Suzuki K, Baba Y, Hasegawa K, Narisawa R, Okada Y, Mizuochi T, Kawachi H, Shimizu F, Asakura H
Third Department of Internal Medicine, Institute of Nephrology, Niigata, Japan.
Clin Immunol. 2000 Oct;97(1):33-42. doi: 10.1006/clim.2000.4909.
LP-BM5 murine leukemia virus (MuLV) is known to induce murine AIDS (MAIDS). We have shown that Sjögren's syndrome (SjS)-like exocrinopathy can be induced in mice with MAIDS and that adoptive transfer of spleen cells from MAIDS mice can induce inflammatory bowel disease-like colitis as well as SjS-like exocrinopathy in nude mice. To assess the role of interferon (IFN)-gamma and interleukin (IL)-10 in the pathogenesis of our experimental model, we tried to identify the cells producing these cytokines and their localization in the colitis lesions in situ. Expression of mRNA for IFN-gamma and IL-10 was assessed by RT-PCR, and protein expression of these cytokines was also analyzed in frozen sections of colon by double-color-staining immunofluorescence (IF). An increase of IFN-gamma and IL-10 mRNA was detected in the colon of mice with colitis, but not in that of control mice. Double-color IF showed that Mac-1(+) cells were positive for IFN-gamma or IL-10 and that most CD4(+) T cells were positive for IL-10, although the population of IFN-gamma-positive CD4(+) T cells was low. In our experimental colitis model, Mac-1(+) macrophages that produce both IFN-gamma and IL-10 might play a crucial role in the pathogenesis of colitis in combination with CD4(+) T cells.
LP - BM5鼠白血病病毒（MuLV）已知可诱发鼠类获得性免疫缺陷综合征（MAIDS）。我们已经表明，在患有MAIDS的小鼠中可诱发类似干燥综合征（SjS）的外分泌腺病，并且将MAIDS小鼠的脾细胞过继转移到裸鼠中可诱发类似炎症性肠病的结肠炎以及类似SjS的外分泌腺病。为了评估干扰素（IFN）-γ和白细胞介素（IL）-10在我们实验模型发病机制中的作用，我们试图鉴定产生这些细胞因子的细胞及其在原位结肠炎病变中的定位。通过逆转录聚合酶链反应（RT-PCR）评估IFN-γ和IL-10的mRNA表达，并且还通过双色染色免疫荧光（IF）在结肠冷冻切片中分析这些细胞因子的蛋白表达。在患有结肠炎的小鼠结肠中检测到IFN-γ和IL-10 mRNA增加，但在对照小鼠结肠中未检测到。双色IF显示，Mac-1(+)细胞对IFN-γ或IL-10呈阳性，并且大多数CD4(+) T细胞对IL-10呈阳性，尽管IFN-γ阳性CD4(+) T细胞群体较少。在我们的实验性结肠炎模型中，产生IFN-γ和IL-10的Mac-1(+)巨噬细胞可能与CD4(+) T细胞一起在结肠炎的发病机制中起关键作用。
