Xabier M G, Howe R C, Frommel D
Armauer Hansen Research Institute (A.H.R.I.), Addis-Abéba, Ethiopie.
C R Acad Sci III. 1992;314(3):99-103.
Previous studies documented that T-cell deficient nude mice failed to control M. leprae infection. In the present investigation we monitored the growth of M. leprae for up to 15 months in the SCID C.B.-17 mouse, a host deficient in both T and B lymphocytes. At 8 months post-infection 10(8) organisms/foot-pad were recovered from SCID mice vs 5 x 10(6) in normal BALB/c mice. Thereafter the number of bacilli decreased rapidly in mice infected with high-dose inoculum (10(7)); however, at all doses SCID mice eventually cleared M. leprae. During infection both T and B cells as well as serum Ig remained as low as in uninfected mice; however, in the spleen MAC-1+ cells which include macrophages and NK cells were substantially increased. These results suggest that MAC-1+ cells are involved in the anti-mycobacteria-1 defence mechanisms adopted by SCID mice to compensate their deficiency in T and B cells.
先前的研究表明,T细胞缺陷的裸鼠无法控制麻风杆菌感染。在本研究中,我们在SCID C.B.-17小鼠(一种T和B淋巴细胞均缺陷的宿主)中监测了麻风杆菌长达15个月的生长情况。感染后8个月,从SCID小鼠的足垫中回收了10(8)个菌/足垫,而正常BALB/c小鼠为5×10(6)个。此后,高剂量接种(10(7))感染的小鼠体内杆菌数量迅速减少;然而,在所有剂量下,SCID小鼠最终都清除了麻风杆菌。在感染期间,T细胞、B细胞以及血清Ig水平与未感染小鼠一样低;然而,脾脏中包括巨噬细胞和NK细胞在内的MAC-1+细胞显著增加。这些结果表明,MAC-1+细胞参与了SCID小鼠为弥补其T和B细胞缺陷而采用的抗分枝杆菌防御机制。