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Impaired Protection against Mycobacterium bovis Bacillus Calmette-Guérin Infection in IL-15-Deficient Mice¹

Kimika Saito^*, Toshiki Yajima^*, Shino Kumabe^*, Takehiko Doi^*, Hisakata Yamada^*, Subash Sad, Hao Shen and Yasunobu Yoshikai^2,*

^* Division of Host Defense, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan; Laboratory of Cellular Immunology, Institute for Biological Sciences, National Research Council of Canada, Ottawa, Ontario, Canada; and Department of Microbiology, School of Medicine, University of Pennsylvania, Philadelphia, PA 19104

To investigate the potential role of endogenous IL-15 in mycobacterial infection, we examined protective immunity in IL-15-deficient (IL-15^–/–) mice after infection with Mycobacterium bovis bacillus Calmette-Guérin (BCG) or recombinant OVA-expressing BCG (rBCG-OVA). IL-15^–/– mice exhibited an impaired protection in the lung on day 120 after BCG infection as assessed by bacterial growth. CD4⁺ Th1 response capable of producing IFN- was normally detected in spleen and lung of IL-15^–/– mice on day 120 after infection. Although Ag-specific CD8 responses capable of producing IFN- and exhibiting cytotoxic activity were detected in the lung on day 21 after infection with rBCG-OVA, the responses were severely impaired on days 70 and 120 in IL-15^–/– mice. The degree of proliferation of Ag-specific CD8⁺ T cells in IL-15^–/– mice was similar to that in wild-type mice during the course of infection with rBCG-OVA, whereas sensitivity to apoptosis of Ag-specific CD8⁺ T cells significantly increased in IL-15^–/– mice. These results suggest that IL-15 plays an important role in the development of long-lasting protective immunity to BCG infection via sustaining CD8 responses in the lung.

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