Izzo A A, North R J
Trudeau Institute, Saranac Lake, New York 12983.
J Exp Med. 1992 Aug 1;176(2):581-6. doi: 10.1084/jem.176.2.581.
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.
去除胸腺的小鼠体内的CD4+ T细胞或CD4+与CD8+ T细胞后,它们无法在其生命、脾脏、肾脏和肺部清除卡介苗(BCG)感染。然而,在卡介苗生长的初始阶段后,这并未使它们无法在这三个器官中稳定感染。无胸腺裸鼠在感染的某个阶段后,在这些器官中显示出类似的控制卡介苗生长的能力。相比之下,先天性严重联合免疫缺陷(SCID)小鼠似乎对卡介苗感染没有抵抗力,因为该病原体在这些小鼠的所有器官中逐渐生长,并且从感染第55天开始对它们具有致死性。结果表明,尽管CD4+ T细胞对于清除卡介苗感染很重要,但在感染2 - 3周时可以获得一种不依赖α/β T细胞的抗性机制,该机制能够抑制除肺部外所有器官中卡介苗的进一步生长。由于SCID小鼠缺乏这种机制,它很可能依赖于γ/δ T细胞、B细胞或这两种细胞的功能。与此可能性相符的是另外一项发现,即移植了去除CD4+或CD8+ T细胞的淋巴结细胞的SCID小鼠能够表达相当水平的抗卡介苗感染能力。