THE CYTOKINE STEW AND INNATE RESISTANCE TO L-MONOCYTOGENES

The Listeria monocytogenes, (L. monocytogenes) infection model has bee n a useful system to evaluate the cellular interactions leading to hos t immunity The initiation of the innate immune response in naive anima ls and subsequent progression to acquired immunity represent an integr ated system with numerous layers of complexity. Coincident with experi mental infection is the induction of cytokines. Cytokines, which are s oluble mediators of cell growth, maintenance and function, form a netw ork of pleiotropic stimuli that serve as one of the main driving force s for the progressive development of cellular responses. A variety of in vivo approaches, such as injection of the recombinant cytokines the mselves or antibodies to neutralize their activity, have been used to define these stimuli. Perhaps one of the most useful tools is that of germline-manipulated animals. One of the many cytokines implicated in resistance to L. monocytogenes infection is interleukin (IL)-6, a mole cule associated with diverse infectious and pathophysiological disease states. This review concentrates on various cytokines (IL-1, TNF alph a, IFN-gamma, IL-12, IL-10 and the colony-stimulating factors (CSF)) t hought to play a role during the innate host response to L. monocytoge nes infection, with a special emphasis on studies using IL-6-deficient mice. Additionally, we show unpublished data obtained when the concep ts learned from L. monocytogenes infection in IL-6-deficient mice were applied to other infection models.