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The Journal of Immunology, Vol 155, Issue 7 3427-3432, Copyright © 1995 by American Association of Immunologists
ARTICLES |
CS Tripp, O Kanagawa and ER Unanue
Center for Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.
During a secondary immune response to Listeria monocytogenes (LM), the production of IFN-gamma was still required for resistance, but it was considerably less dependent on IL-12 production. When IL-12 was neutralized in vivo using specific hamster antimurine IL-12 mAbs, there was a dramatically increased susceptibility to infection during primary listeriosis but much less during a secondary infection. However, neutralization of IFN-gamma in vivo resulted in a similar increased susceptibility during both primary and secondary listeriosis. In culture, splenocytes isolated from unimmunized mice produced IFN-gamma in response to heat-killed L. monocytogenes (hk-LM) that was absolutely dependent upon IL-12 production. However, directly stimulating the TCR with anti-CD3-epsilon mAbs resulted in IFN-gamma production that was unaffected by neutralizing IL-12 in vitro. In contrast, splenocytes isolated from LM-immune mice produced IFN-gamma in response to hk-LM, part of which was independent on IL-12 production. However, anti-CD3- epsilon Ab-stimulated IFN-gamma production remained independent of IL- 12 production. The source of hk-LM-induced, IL-12-independent IFN-gamma production was the T cell because anti-Thy1.2 Ab plus complement treatment in vitro completely abolished it. Together, these data support a model of memory T cells being produced during the primary infection with LM that can be stimulated to produce IFN-gamma during the secondary response to LM, partially independent of macrophage IL-12 production.
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