NK cell-mediated killing?

Klaus D. Elgert kdelgert at vt.edu
Wed Dec 27 14:19:02 EST 2000

In the midst of the holiday cheer, would some NK cell gurus help 
clarify stuff to a macrophage person?  The following questions arose 
during a debate/discussion we had in a graduate immunology course.

Literature suggests that the NK cell's ability to recognize and kill 
a virally infected target cell depends on the integrity and amount of 
target cell surface class I MHC proteins.  This integrity and amount 
of surface class I MHC proteins determine whether the NK cell's 
inhibitory or activating receptor signals prevail.  Given that 
scenario, what is the mechanism by which NK cells distinguish class I 
MHC carrying self-peptides from class I MHC carrying viral derived 
peptides?  In particular, if the virally infected target cell's 
amount and class I MHC molecule integrity are normal (as cells 
targeted by cytotoxic T lymphocytes [CTLs]), do/can NK cells kill 
this target cell?  In more technical terms, if NK cells recognize 
class I MHC molecules displaying self-peptides as a "no kill" ligand 
would the replacement of self-peptide with viral peptide in class I 
MHC molecules be enough to cause a failure to nullify the "kill" 
signal?  Or do NK cells only kill virally infected cells that have 
altered class I MHC molecules or reduced (or inhibited) expression of 
class I MHC molecules?  If the answer to the last question were yes, 
then it would be wrong to say, at least in a generic way, that all 
cells infected by virus activate NK cells?  The flipside would be 
that all virus-infected cells must have either altered (does every 
molecule have to be changed?) and/or reduced or inhibited expression 
of class I MHC molecules for NK cells to recognize and kill the 
virus-infected cells.  So if MHC things are "normal" on a 
virus-infected cell, only CTLs work.  If MHC things are "abnormal" on 
a virus-infected cell, only NK cells work.



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