Abstract
1. Mechanisms of host defense and granulomatous inflammation in acid-fast bacilli Infection: Kazuo KOBAYASHI (Leprosy Res. Ctr., Ntnl. Inst. Infec. Dis.)
2. Induction and function of Th 1 cells as the effector cells in anti-tuberculosis immunity: Masao MITSUYAMA (Niigata Univ. Sch. Med.)
3. Role of γ/δ cells in tuberculous infection: Chisato UETA (Osaka Perfectural Habikino Hospital)
4. Role of immune responses in tuberculosis: Discussion from clinical observations: Katsuhiro SUZUKI (Chest Dis. Res. Inst., Kyoto Univ.)
5. Merit and demerit of cytokines in the prevention and treatment of tuberculosis: Kazuyoshi KAWAKAMI (Ryukyu Univ. Sch. Med.)
Tuberculosis is considered in general a chronic infectious disease caused by Mycobacterium tuberculosis. However, major pathological lesions of the disease are induced by host immune responses to tubercle bacilli. In most other infectious diseases, the interaction between invading pathological organisms and host defense mechanism would determine the outcome of the invasion; whether or not the onset of illness does follow the infection. In tuberculosis, however, this pattern of the pathogenesis is not necessarily followed. In fact, a highly immunogenic epitope from tubercle bacilli does not necessarily represent the best candidate of the effective vaccines for tuberculosis. Thus, this symposium was now organized when the detailed immune responses in human tuberculosis have not yet been revealed completely. In other words, our aim of the symposium is to understand how much the studies on tuberculous immunity have revealed the host defense mechanisms against tuberculosis.
We have asked both Drs. Kobayashi and Mitsuyama to present their views to what extent we could extrapolate the data obtained from in vitro and in vivo studies on murine experimental infection with acid-fast bacilli for future prevention and treatment of the tuberculosis in man. Firstly, Dr. Kobayashi presented the data indicating that murine strain susceptible to MAC infection are not capable of generating IL12 and also that the death due to MAC infection can be prevented by administration of exogenous IL12 to these susceptible mice. In discussion for the implication of these data, he has suggested that the future challenge in establishing anti-tuberculous immunotherapies with IL12 would be how to control the organ damages induced by such treatment.
Dr. Mitsuyama has shown that NK cell-dependent IFN- γ appeared to be critically important in the generation of antigen- specific (protective) TH 1 cells at the early stage of immune response to viable virulent bacteria. Several cytokines such as IL12 and IL18 released from macrophages seem to be essential in the stimulation of NK cells to produce IFN γ. He strongly suggested that these experimental findings should be confirmed by studies in man using human clinical samples.