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首页> 外文期刊>The Journal of Experomental Medicine >Evidence for an alpha/beta T cell-independent mechanism of resistance to mycobacteria. Bacillus-Calmette-Guerin causes progressive infection in severe combined immunodeficient mice, but not in nude mice or in mice depleted of CD4+ and CD8+ T cells.
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Evidence for an alpha/beta T cell-independent mechanism of resistance to mycobacteria. Bacillus-Calmette-Guerin causes progressive infection in severe combined immunodeficient mice, but not in nude mice or in mice depleted of CD4+ and CD8+ T cells.

机译:对分枝杆菌耐药的独立于α/βT细胞的机制的证据。芽孢杆菌-Calmette-Guerin会在严重的合并免疫缺陷小鼠中引起进行性感染,但在裸鼠或CD4 +和CD8 + T细胞耗尽的小鼠中不会引起感染。

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Depleting thymectomized mice of CD4+ T cells, or CD4+ plus CD8+ T cells, rendered them incapable of resolving Bacillus-Calmette-Guerin (BCG) infection in their lives, spleens, kidneys, and lungs. However, it did not render them incapable of stabilizing infection in the latter three organs after an initial period of BCG growth. Athymic nude mice showed a similar capacity to control BCG growth in these organs after a certain stage of infection. In contrast, congenitally severe combined immunodeficient (SCID) mice appeared to offer no resistance to BCG infection, in that the organism grew progressively in all organs of these mice and was lethal for them beginning on day 55 of infection. The results suggest that, although CD4+ T cells are important for resolving BCG infection, an alpha/beta T cell-independent mechanism of resistance can be acquired at 2-3 wk of infection that is capable of inhibiting further BCG growth in all organs except the lungs. Because this mechanism is absent from SCID mice, it is likely that it depends on the functions of gamma/delta T cells, B cells, or both types of cells. In keeping with this possibility is the additional finding that SCID mice engrafted with lymph node cells depleted of CD4+ or CD8+ T cells were capable of expressing an appreciable level of resistance against BCG infection.
机译:去除CD4 + T细胞或CD4 +加CD8 + T细胞的经胸腺切除的小鼠,使其无力解决其芽孢杆菌,卡尔梅特-娇兰(BCG)感染的生活,脾脏,肾脏和肺部感染。然而,它并没有使它们在卡介苗生长初期后就无法稳定后三个器官的感染。在感染一定阶段后,无胸腺裸鼠显示出类似的控制这些器官中BCG生长的能力。相反,先天性严重的联合免疫缺陷(SCID)小鼠似乎对BCG感染没有抵抗力,因为该微生物在这些小鼠的所有器官中均逐渐生长,并在感染第55天开始致死。结果表明,尽管CD4 + T细胞对于解决BCG感染很重要,但在感染后2-3 wk仍可获得不依赖于α/βT细胞的耐药机制,该机制能够抑制除BCG以外的所有器官中BCG的进一步生长。肺。因为SCID小鼠缺乏这种机制,所以它可能取决于γ/δT细胞,B细胞或两种细胞的功能。与这种可能性保持一致的另一个发现是,植入了耗尽了CD4 +或CD8 + T细胞的淋巴结细胞的SCID小鼠能够表达对BCG感染的明显抵抗力。

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