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It lives primarily as an extracellular pathogen, although in vitro it can also hide intracellularly (see Mechanisms of persistence section).
In 2004, a novel third function was identified: formation of NETs, whereby neutrophils kill extracellular pathogens while minimizing damage to the host cells.
This is important because one of the primary functions of T cells is to identify and respond to infected host cells as opposed to extracellular pathogens.
Interleukin 17 as a family functions as a proinflammatory cytokine that responds to the invasion of the immune system by extracellular pathogens and induces destruction of the pathogen's cellular matrix.
In contrast, MHC Class II genes are responsible for the destruction of extracellular pathogens; these types of pathogens are either phagocytized by macrophages or bound by antibodies.
Because class II MHC is loaded with extracellular proteins, it is mainly concerned with presentation of extracellular pathogens (for example, bacteria that might be infecting a wound or the blood).
Homologs of LcrG and LcrV (i.e., PcrG and PcrV) have only been identified in P. aeruginosa, suggesting that this pair of regulatory proteins may fulfill similar roles in these extracellular pathogens.
Staphylococci have typically been regarded as non-invasive extracellular pathogens that damage host cells after adhering to the extracellular matrix; however, there is growing evidence that S. aureus has the ability to invade and persist within eukaryotic cells.