Interaction between intracellular pathogens and host follows different pathways which reflect evolved survival mechanisms of both the pathogen and the host to assure each one's own survival. Different immune mechanisms dominate at different stages of infection. Both phagocytic and non-phagocytic target cells participate in microbial uptake and, in some cases, intracellular destruction. Resistance to intracellular bacterial infections involves almost all the components of the immune system. The development of specific immunity ensures sustained activation of intracellular microbicidal mechanisms in the target cells, and induction of apoptotic or lytic target cell death by cytotoxic T lymphocytes.

The inflammatory response is triggered initially by nonspecific mechanisms, and then by the interaction between T-cell receptors and bacterial antigens. Characterization of bacterial antigens able to induce protective immunity would be of great value to improve vaccination strategies.

A compromised immune system, an altered microbiota, or breached skin or mucosal barriers allow these microorganisms the opportunity to cause infections. Their ability to persist and to be transmitted without detection gives such opportunistic pathogens a unique disease biology that warrants special attention.

The function of adaptive immune responses is to destroy invading pathogens and any toxic molecules they produce. Because these responses are destructive, it is crucial that they be made only in response to molecules that are foreign to the host and not to the molecules of the host itself. The ability to distinguish what is foreign from what is self in this way is a fundamental feature of the adaptive immune system. Occasionally, the system fails to make this distinction and reacts destructively against the host's own molecules. Such autoimmune diseases can be fatal.

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