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Self-MHC class Ia (RT1-A(n)) protects cells co-expressing the activatory allogeneic MHC class Ib molecule (RT1-E(u)) from NK lysis.

Authors: Backman-Petersson, E  Butcher, GW  Hedlund, G 
Citation: Backman-Petersson E, etal., Int Immunol. 2000 Jun;12(6):843-50.
Pubmed: (View Article at PubMed) PMID:10837412

We have previously shown activation of NK cells via recognition of an allogeneic, non-classical MHC class I molecule, RT1-E(u). In this study we investigated whether a self-MHC class I molecule could protect the allogeneic targets from being recognized and killed by the alloreactive NK (allo NK) cells. NK cells from BN (RT1 n) rats, primed in vivo by immunization with RT1(u)-expressing cells, manifested cytolytic activity against RT1(u)- as well as RT1(u/lv1)-expressing targets, but not against RT1(u/n)-expressing targets. The absence of cytolytic activity against semiallogeneic targets, i.e. targets expressing self-allotypes, was also valid for allo NK cells from alloimmunized F344 (RT1 (lv1)) rats. To analyze the ability of a distinct MHC class I molecule to protect target cells from NK lysis, Rat2 cells transfected with the activating allogeneic MHC class Ib, RT1-E(u) molecule were also transfected with the self-MHC class Ia, RT1-A1(n) molecule. The allo NK cells from BN rats immunized with RT1(u)-expressing cells were cytolytic against Rat2 transfected with the RT1-E(u) molecule. However, the allo NK cells manifested no cytolytic activity against double-transfected Rat2 cells, expressing the RT1-E(u) as well as the RT1-A1(n) molecule. We conclude that expression of a self-MHC class Ia (RT1-A) molecule protects targets from allo NK killing. Furthermore, the NK inhibition via recognition of the self-MHC class Ia molecule dominates over the activation via recognition of the allogeneic MHC class Ib molecule, RT1-E.

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CRRD Object Information
CRRD ID: 2313500
Created: 2009-09-29
Species: All species
Last Modified: 2009-09-29
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.