ABSTRACT
Most infectious diseases suffered by humans are caused by pathogens much smaller than a human cell. For these microbes, the human body constitutes a vast resource-rich environment in which to live and reproduce. In facing such threats, the body deploys a variety of defense mechanisms that have accumulated over hundreds of millions of years of invertebrate and vertebrate evolution. In considering mechanisms of innate immunity in Chapters 2 and 3 and of adaptive immunity in Chapters 4-11, we principally used the example of a bacterial pathogen that enters the body through a skin wound, causing an innate immune response in the infected tissue that then leads to an adaptive immune response in the draining lymph node. The merits of this example are that it is simple and involves a tissue for which we have all observed the effects of wounds, infection, and inflammation. Until recently, these were the only responses studied by most immunologists, who usually administered their experimental antigens by subcutaneous injection. But in the real world, only a fraction of human infections are caused by pathogens that enter the body’s tissues by passage through the skin. Many more infections, including all of those caused by viruses, make their entry by passage through one of the mucosal surfaces. Although the immune response to infection of mucosal tissue has strategies and principles in common with those directed at infections of skin and connective tissue, there are important differences, both in the cells and molecules involved, as well as the ways in which they are used. Appreciation of the extent of these differences has led to the concept that the human immune system actually consists of two semi-autonomous parts: the systemic immune system, which defends against pathogens penetrating the skin, and the mucosal immune system, which defends against pathogens breaching mucosal surfaces. This chapter focuses on mucosal immunity and how it differs from systemic immunity.
