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2014 ; 26
(2
): 138-44
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NK cell self tolerance, responsiveness and missing self recognition
#MMPMID24629893
Shifrin N
; Raulet DH
; Ardolino M
Semin Immunol
2014[Apr]; 26
(2
): 138-44
PMID24629893
show ga
Natural killer (NK) cells represent a first line of defense against pathogens and
tumor cells. The activation of NK cells is regulated by the integration of
signals deriving from activating and inhibitory receptors expressed on their
surface. However, different NK cells respond differently to the same stimulus, be
it target cells or agents that crosslink activating receptors. The processes that
determine the level of NK cell responsiveness have been referred to collectively
as NK cell education. NK cell education plays an important role in steady state
conditions, where potentially auto-reactive NK cells are rendered tolerant to the
surrounding environment. According to the "tuning" concept, the responsiveness of
each NK cell is quantitatively adjusted to ensure self tolerance while at the
same time ensuring useful reactivity against potential threats. MHC-specific
inhibitory receptors displayed by NK cells play a major role in tuning NK cell
responsiveness, but recent studies indicate that signaling from activating
receptors is also important, suggesting that the critical determinant is an
integrated signal from both types of receptors. An important and still unresolved
question is whether NK cell education involves interactions with a specific cell
population in the environment. Whether hematopoietic and/or non-hematopoietic
cells play a role is still under debate. Recent results demonstrated that NK cell
tuning exhibits plasticity in steady state conditions, meaning that it can be
re-set if the MHC environment changes. Other evidence suggests, however, that
inflammatory conditions accompanying infections may favor high responsiveness,
indicating that inflammatory agents can over-ride the natural tendency of NK
cells to adjust to the steady state environment. These findings raise many
questions such as whether viruses and tumor cells manipulate NK cell
responsiveness to evade immune-recognition. As knowledge of the underlying
processes grows, the possibility of modulating NK cell responsiveness for
therapeutic purposes is becoming increasingly attractive, and is now under
serious investigation in clinical studies.
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