Interleukin-6 induces early gamma interferon production in the infected lung but is not required for generation of specific immunity to Mycobacterium tuberculosis infection
Interleukin-6 induces early gamma interferon production in the infected lung but is not required for generation of specific immunity to Mycobacterium tuberculosis infection
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DOI：
10.1128/iai.68.6.3322-3326.2000
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发表时间：
2000-06-01
影响因子：
3.1
通讯作者：
Cooper, AM
中科院分区：
文献类型：
--
作者：
Saunders, BM;Frank, AA;Cooper, AM
对结核分枝杆菌的免疫力依赖于产生保护性γ干扰素（IFN-γ）的T细胞应答。最近的研究表明，白细胞介素-6（IL-6）是诱导保护性T细胞应答所必需的，而IL-4可抑制IFN-γ的诱导。IL-6和IL-4基因敲除小鼠感染结核杆菌，用M.肺结核放射免疫气雾剂IL-6的缺乏导致细菌负荷的早期增加，同时延迟IFN-γ的诱导。然而，小鼠能够抑制和控制细菌生长，并对继发感染产生保护性记忆反应。这表明，虽然IL-6参与刺激早期IFN-γ产生，但它对于产生针对M.结核相反，虽然IL-4的缺乏导致IFN-γ产生增加，但这对细菌生长没有显著影响。
Immunity to Mycobacterium tuberculosis is dependent upon the generation of a protective gamma interferon (IFN-gamma)-producing T-cell response. Recent studies have suggested that interleukin-6 (IL-6) is required for the induction of a protective T-cell response and that IL-4 may suppress the induction of IFN-gamma, To evaluate the role of the cytokines IL-6 and IL-4 in the generation of pulmonary immunity to M. tuberculosis, IL-6 and IL-4 knockout mice were infected,vith M. tuberculosis ria aerosol. The absence of IL-6 led to an early increase in bacterial load with a concurrent delay in the induction of IFN-gamma. However, mice were able to contain and control bacterial growth and developed a protective memory response to secondary infection, This demonstrates that while IL-6 is involved in stimulating early IFN-gamma production, it is not essential for the development of protective immunity against M. tuberculosis. In contrast, while the absence of IL-4 resulted in increased IFN-gamma production, this had no significant effect upon bacterial growth.