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Innate Immunity in Bacterial Infections, Page 1 of 2
< Previous page Next page > /docserver/preview/fulltext/10.1128/9781555817978/9781555812140_Chap07-1.gif /docserver/preview/fulltext/10.1128/9781555817978/9781555812140_Chap07-2.gifAbstract:
The host response to pathogens is extraordinarily diverse. Much of the host response centers on the pathogen and the route and extent of the infection. This chapter analyzes some general features of host-pathogen interaction and discusses general principles of them. The chapter is based on a recent one that also dealt with general aspects of innate immunity and considered aspects of innate immunity studied mainly in mice. While many bacterial infections can be controlled, SCID mice do not do well in combating viruses. Infections with common murine pathogens, including viruses, and other pathogens, like Pneumocystis carinii, occasionally develop. The state of cellular activation is limited and cannot be perpetuated unless lymphocytes are present. The innate system recognizes pathogens by way of surface receptors as well as by using circulating blood proteins. A variety of surface molecules, found mostly in macrophages and neutrophils but also in epithelial cells, are involved: some primarily recognize and bind to the pathogen, and others are primarily involved in signaling or in promoting phagocytosis. The production and differentiation of macrophages are under the control of colony-stimulating factors (CSF), of which CSF-1 is the major member. CSF-1 is a protein elaborated by many cells including mesenchymal cells. T-cell responses depend on their recognition of peptides derived from the intracellular processing of protein antigens, an event carried out by the macrophages or DC, major cells of the innate system.