There are several theories as to how new effector cells

are generated from memory cells when needed, and it is likely that all of these mechanisms play a role in immunological protection. One possibility is that short-lived effector cells are produced continuously by memory cell division, replacing the older cells of the same specificity – this process would be driven by the persistence of antigen. Long-lived effector cells may also be generated from memory cells in a process driven by cytokines and engagement of PRRs in response to a new encounter with the pathogen. A third possibility is that effector cells remain for long periods in specialised survival niches Cabozantinib molecular weight – there is some evidence that this is an important mechanism in B-cell memory, since depletion of memory B cells does not significantly impact the level of circulating antibodies, probably due to the presence of long-lived plasma cells. As we have seen, the innate and adaptive immune systems occupy

distinct evolutionary and functional niches. The innate immune system, along with physical and chemical barriers, provides a first line of defence against invasion or damage. A system RAD001 chemical structure of cellular and soluble mediators then transmits the nature of the threat to the adaptive immune system, which selectively expands the appropriate repertoire in order to deal with the threat. The key differences between these two systems are summarised in Table 2.2. In the next section, the mechanisms linking innate and adaptive immunity will be discussed. As previously discussed, the innate immune system provides an essential

link between the first encounter with a pathogen at the site of infection and the eventual establishment of immune memory. Innate cells (such as macrophages and DCs) are strategically located at body sites with a high risk of infection (such as epithelia and mucosal surfaces). These types of cells act as both a first line of defence against danger and as key messengers that are able to alert the adaptive immune system. Since naïve T and B cells Histamine H2 receptor are not pre-positioned in most organs and tissues of the body, they rely on the innate immune system to sense an infectious event. Among tissue-resident cells, the most efficient APCs are DCs. Immature DCs which have captured antigen become activated and mature into functional APCs, while migrating to the regional draining lymph node or submucosal lymphoid tissue. Mature DCs express high levels of antigen/MHC complexes at the cell surface and undergo morphological changes, which render them highly specialised, to activate naïve T cells. When they arrive in the lymph node, DCs present processed antigen and express co-stimulatory signals.