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The Journal of Immunology, Vol 142, Issue 4 1134-1138, Copyright © 1989 by American Association of Immunologists
ARTICLES |
J Goronzy, C Weyand, J Quan, CG Fathman and P O'Hanley
Department of Medicine, Stanford University Medical Center, CA 94305.
Administration of rIL-2 to BALB/c mice induces a rapid, cell-mediated response that is sufficient to protect mice from a lethal i.p. dose of Escherichia coli. Mice were protected from septic death if IL-2 was administered i.p. within 1 h after the bacterial challenge. Optimal protection was provided by treating the lethally challenged mice with rIL-2 at 1 and 5 h or 1, 5, and 10 h after the bacterial challenge and was dose-dependent (greater than or equal to 5.0 x 10(5) U/kg). Furthermore, treatment of mice with anti-IL-2R antibody abolished the protective effect induced by rIL-2 administration. These data suggest that the rIL-2-induced protection against septic death in mice is mediated by a cell type expressing a functional IL-2R. One potentially important therapeutic application of rIL-2 may be to modulate the course of sepsis once the host has been exposed to potentially lethal microbial pathogens.
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