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* Laboratory of Host Defense, Research Institute for Disease Mechanism and Control, Nagoya University School of Medicine
Department of Bacteriology, National Institute of Infectious Diseases, Tokyo
Department of Pathology, Faculty of Veterinary Medicine, Kasetsart University, Nakhonpathom, Thailand
Department of Veterinary Microbiology, Faculty of Agriculture, Miyazaki University, Japan
|| Center of Excellence, Department of Pathology II, Nagoya University School of Medicine, Japan
# Division of Human Retrovirus, Center for Chronic Viral Diseases, Faculty of Medicine, Kagoshima University, Japan
Correspondence: Yasunobu Yoshikai, M.D., Ph.D., Laboratory of Host Defense, Research Institute for Disease Mechanism and Control, Nagoya University School of Medicine, Nagoya 466-8550, Japan. E-mail: yyoshika{at}tsuru.med.nagoya-u.ac.jp
LP-BM5 murine leukemia virus (MuLV) injection causes murine AIDS (MAIDS), a disease characterized by many functional abnormalities of immunocompetent cells. We show that MAIDS mice are susceptible to Mycobacterium bovis Bacille Calmette-Guérin (BCG) infection as assessed by survival rate and bacterial counts. The peritoneal exudate macrophages from MAIDS mice produced a significant level of interleukin (IL)-12 soon after inoculation with BCG, whereas IL-15 and tumor necrosis factor (TNF) production were severely impaired in BCG-infected MAIDS mice. The appearance of natural killer (NK) and CD4+ T helper type 1 (Th1) cells specific for mycobacterial antigen were depressed in MAIDS mice after BCG infection. Thus, it appeared that impaired production of IL-15, besides other inflammatory cytokines, in MAIDS mice may be involved in the poor responses of the NK and Th1 cells, resulting in an increased susceptibility to BCG.
Key Words: interleukin-15 macrophages interferon-
T helper type1 cells infectious immunity Mycobacterium bovis BCG
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