Ellner J J
Case Western Reserve University, Division of Infectious Diseases, University Hospitals, Cleveland, Ohio 44106.
Bull Int Union Tuberc Lung Dis. 1991 Jun-Sep;66(2-3):129-32.
After infection with M. tuberculosis, about 5% of individuals develop progressive tuberculosis during the following two years and an additional 5% delayed reactivation. The genetic and acquired factors which place individuals at risk of tuberculosis are partly defined; however, the connection of the susceptibility to the host immune response is much less clear. Recent studies have examined the basis for the immunosuppression that is a concomitant of tuberculosis. Direct stimulation of monocytes primed during the course of tuberculous infection by mycobacterial peptides appears to be responsible for suppression of PPD-induced responses. Increased expression and release of interleukin-2 receptors and transforming growth-factor beta are associated with and may contribute to such suppression by monocytes. Additional studies have addressed the generation of immunity or immunosuppression. Ingestion of live M. tuberculosis by monocytes leads to selective expansion of gamma-delta T cells as opposed to CD4 lymphocytes. This may be relevant to the innate response to infection with M. tuberculosis as well as immunoregulatory circuits. Increased understanding of the basis for immunosuppression is of intrinsic interest as regards regulation of specific pathways of immune reactivity in an infectious disease of humans and may provide some insight into factors predisposing to tuberculosis.
感染结核分枝杆菌后，约5%的个体在接下来的两年内会发展为进行性结核病，另有5%会出现延迟再激活。使个体面临结核病风险的遗传和后天因素已部分明确；然而，易感性与宿主免疫反应之间的联系却不太清楚。最近的研究探讨了与结核病相伴的免疫抑制的基础。结核感染过程中被分枝杆菌肽致敏的单核细胞受到直接刺激似乎是PPD诱导反应受到抑制的原因。白细胞介素-2受体和转化生长因子β的表达及释放增加与单核细胞的这种抑制作用相关且可能促成这种抑制。其他研究探讨了免疫或免疫抑制的产生。单核细胞摄取活的结核分枝杆菌会导致γ-δT细胞而非CD4淋巴细胞选择性扩增。这可能与对结核分枝杆菌感染的固有反应以及免疫调节回路有关。对于人类传染病中免疫反应特定途径的调节而言，对免疫抑制基础的深入了解本身就很有意义，并且可能为易患结核病的因素提供一些见解。
