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The Journal of Immunology, Vol 156, Issue 2 663-669, Copyright © 1996 by American Association of Immunologists
ARTICLES |
H Nishimura, K Hiromatsu, N Kobayashi, KH Grabstein, R Paxton, K Sugamura, JA Bluestone and Y Yoshikai
Laboratory of Host Defense and Germfree Life, Nagoya University School of Medicine, Japan.
We have previously shown evidence for the early recruitment of gamma delta T cells during the disease course of primary infections with Listeria monocytogenes or Salmonella choleraesuis in mice. Since gamma delta T cells at this stage of the disease do not produce IL-2, the growth factor for the gamma delta T cells remains unknown. IL-15 is a novel cytokine that uses beta- and gamma-chain of IL-2R for signal transduction, and is produced by activated monocytes/macrophages. In this study, we investigated the proliferative activity of IL-15 for gamma delta T cells appearing after primary infection with S. choleraesuis 31N-1. The gamma delta T cells, which expressed beta- and gamma-chains of IL-2R, proliferated in the presence of rIL-15 and produced appreciable levels of gamma-IFN and IL-4. Addition of anti-IL- 2R beta mAb significantly inhibited the IL-15-induced proliferation of the gamma delta T cells. Furthermore, the gamma delta T cells produced gamma-IFN in response to monocyte/macrophage cell line, J774A.1 infected with S. choleraesuis, which expressed an abundant level of IL- 15 mRNA. This cytokine production was inhibited significantly by anti- IL-15 Ab. Taken together, these results suggest that IL-15 derived from infected macrophages may contribute to the early activation of gamma delta T cells during salmonellosis.
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