Flesch I E, Kaufmann S H
Department of Medical Microbiology and Immunology, University of Ulm, Federal Republic of Germany.
Infect Immun. 1990 Aug;58(8):2675-7. doi: 10.1128/iai.58.8.2675-2677.1990.
The capacity of the cytokines gamma interferon (IFN-gamma), interleukin-4 (IL-4), and tumor necrosis factor (TNF) to activate tuberculostatic functions in murine bone marrow-derived macrophages (BMM phi) was investigated. In confirmation of earlier findings, IFN-gamma rendered BMM phi capable of inhibiting subsequent infection with Mycobacterium bovis. In contrast, IL-4 and TNF failed to inhibit mycobacterial growth. However, in already infected BMM phi, tuberculostasis was induced by subsequent stimulation with IL-4. Although TNF alone was ineffective, it showed synergy with IFN-gamma in the stimulation of tuberculostasis. Our data suggest that not only IFN-gamma but also IL-4 and TNF participate in the control of mycobacterial growth.
研究了细胞因子γ干扰素（IFN-γ）、白细胞介素-4（IL-4）和肿瘤坏死因子（TNF）激活小鼠骨髓来源巨噬细胞（BMMφ）中结核菌抑制功能的能力。正如早期研究结果所证实的，IFN-γ使BMMφ能够抑制随后的牛分枝杆菌感染。相比之下，IL-4和TNF未能抑制分枝杆菌生长。然而，在已经感染的BMMφ中，随后用IL-4刺激可诱导结核菌抑制。虽然单独的TNF无效，但它在刺激结核菌抑制方面与IFN-γ显示出协同作用。我们的数据表明，不仅IFN-γ，而且IL-4和TNF都参与了对分枝杆菌生长的控制。
