Satoskar A R, Okano M, Connaughton S, Raisanen-Sokolwski A, David J R, Labow M
Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston 02115, USA.
Eur J Immunol. 1998 Jul;28(7):2066-74. doi: 10.1002/(SICI)1521-4141(199807)28:07<2066::AID-IMMU2066>3.0.CO;2-X.
IL-1 has a number of effects on T cell growth but a specific role for IL-1 in T cell responses in vivo has not been elucidated. In this study the role of IL-1 in Th1/Th2 responses was examined in mice deficient for the IL-1 type 1 receptor (IL-1RI-/-) during cutaneous Leishmania major infection or following immunization with keyhole limpet hemocyanin (KLH). After inoculation of L. major stationary phase promastigotes into the hind footpad, both IL-1RI-/- and wild-type (WT) mice developed small lesions which resolved spontaneously. Lymph node cells from infected IL-1RI-/- mice produced significantly more IL-4 and IL-10 than those from WT mice following antigenic stimulation in vitro. Splenocytes from IL-1RI-/- and WT mice showed similar levels of antigen-induced proliferation. In contrast, splenocyte cultures from the IL-1RI-/- mice contained significantly more IL-4 than those from WT mice. Similar results were also obtained after immunization with KLH. While lymph node cells from both IL-1RI-/- and WT mice displayed similar levels of KLH-specific proliferation, those from IL-1RI-/- mice produced significantly more IL-4 than those from WT mice. Conversely, antigen-stimulated lymph node cells from WT mice secreted significantly greater amounts of IFN-gamma as compared with those from IL-1RI-/- mice. These data indicate that while IL-1 is not required for mounting an immune response or antigen-dependent proliferation, it appears to be required for normal regulation of Th1/Th2 responses and may function to negatively regulate IL-4 expression.
白细胞介素-1（IL-1）对T细胞生长有多种作用，但IL-1在体内T细胞应答中的具体作用尚未阐明。在本研究中，在皮肤利什曼原虫主要感染期间或用钥孔戚血蓝蛋白（KLH）免疫后，在缺乏白细胞介素-1 1型受体（IL-1RI-/-）的小鼠中研究了IL-1在Th1/Th2应答中的作用。将利什曼原虫主要静止期前鞭毛体接种到后足垫后，IL-1RI-/-和野生型（WT）小鼠均出现小病变，这些病变可自发消退。在体外抗原刺激后，来自感染的IL-1RI-/-小鼠的淋巴结细胞产生的IL-4和IL-10明显多于WT小鼠。来自IL-1RI-/-和WT小鼠的脾细胞显示出相似水平的抗原诱导增殖。相反，来自IL-1RI-/-小鼠的脾细胞培养物中IL-4含量明显高于WT小鼠。用KLH免疫后也得到了类似的结果。虽然来自IL-1RI-/-和WT小鼠的淋巴结细胞显示出相似水平的KLH特异性增殖，但来自IL-1RI-/-小鼠的细胞产生的IL-4明显多于WT小鼠。相反，与来自IL-1RI-/-小鼠的细胞相比，WT小鼠抗原刺激的淋巴结细胞分泌的干扰素-γ量明显更多。这些数据表明，虽然启动免疫应答或抗原依赖性增殖不需要IL-1，但它似乎是Th1/Th2应答正常调节所必需的，并且可能起到负调节IL-4表达的作用。
