Ladel C H, Blum C, Dreher A, Reifenberg K, Kaufmann S H
Department of Immunology, University of Ulm, Germany.
Eur J Immunol. 1995 Oct;25(10):2877-81. doi: 10.1002/eji.1830251025.
Tuberculosis is a chronic infectious disease which causes major health problems globally. Although acquired resistance crucially depends on alpha/beta lymphocytes, circumstantial evidence suggests that, in addition, gamma/delta T lymphocytes contribute to protection against tuberculosis. We have studied Mycobacterium tuberculosis infection in TcR-delta-/- or TcR-beta-/- gene deletion mutants which completely lack gamma/delta T cells or alpha/beta T cells, respectively. Low inocula of M. tuberculosis led to death of TcR-beta-/- mice and transient disease exacerbation in TcR-delta-/- mutants. Infection with higher inocula caused rapid death of TcR-delta-/- mice. The development of and bacterial containment in granulomatous lesions was markedly impaired in TcR-beta-/-, and less severely affected in TcR-delta-/- mutants. Mycobacteria-induced IFN-gamma production by spleen cells in vitro was almost abolished in TcR-beta-/- and virtually unaffected in TcR-delta-/- mice. Our data confirm the crucial role of alpha/beta T cells in protection against established tuberculosis and formally prove a protective role of gamma/delta T cells in early tuberculosis.
结核病是一种慢性传染病,在全球范围内引发了重大的健康问题。尽管获得性耐药主要取决于α/β淋巴细胞,但间接证据表明,γ/δ T淋巴细胞也有助于抵御结核病。我们研究了TcR-δ-/-或TcR-β-/-基因缺失突变体中的结核分枝杆菌感染情况,这些突变体分别完全缺乏γ/δ T细胞或α/β T细胞。低剂量的结核分枝杆菌接种导致TcR-β-/-小鼠死亡,而在TcR-δ-/-突变体中则导致短暂的疾病加重。高剂量接种感染导致TcR-δ-/-小鼠迅速死亡。肉芽肿性病变的形成和细菌控制在TcR-β-/-小鼠中明显受损,而在TcR-δ-/-突变体中受到的影响较小。在体外,结核分枝杆菌诱导的脾细胞产生IFN-γ在TcR-β-/-小鼠中几乎完全被消除,而在TcR-δ-/-小鼠中几乎不受影响。我们的数据证实了α/β T细胞在抵御已建立的结核病中的关键作用,并正式证明了γ/δ T细胞在早期结核病中的保护作用。