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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Front+Immunol
2017 ; 8
(ä): 166
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Dual Role of Natural Killer Cells on Graft Rejection and Control of
Cytomegalovirus Infection in Renal Transplantation
#MMPMID28261220
López-Botet M
; Vilches C
; Redondo-Pachón D
; Muntasell A
; Pupuleku A
; Yélamos J
; Pascual J
; Crespo M
Front Immunol
2017[]; 8
(ä): 166
PMID28261220
show ga
Allograft rejection constitutes a major complication of solid organ
transplantation requiring prophylactic/therapeutic immunosuppression, which
increases susceptibility of patients to infections and cancer. Beyond the pivotal
role of alloantigen-specific T cells and antibodies in the pathogenesis of
rejection, natural killer (NK) cells may display alloreactive potential in case
of mismatch between recipient inhibitory killer-cell immunoglobulin-like
receptors (KIRs) and graft HLA class I molecules. Several studies have addressed
the impact of this variable in kidney transplant with conflicting conclusions;
yet, increasing evidence supports that alloantibody-mediated NK cell activation
via Fc?RIIIA (CD16) contributes to rejection. On the other hand, human
cytomegalovirus (HCMV) infection constitutes a risk factor directly associated
with the rate of graft loss and reduced host survival. The levels of
HCMV-specific CD8(+) T cells have been reported to predict the risk of
posttransplant infection, and KIR-B haplotypes containing activating KIR genes
have been related with protection. HCMV infection promotes to a variable extent
an adaptive differentiation and expansion of a subset of mature NK cells, which
display the CD94/NKG2C-activating receptor. Evidence supporting that adaptive
NKG2C(+) NK cells may contribute to control the viral infection in kidney
transplant recipients has been recently obtained. The dual role of NK cells in
the interrelation of HCMV infection with rejection deserves attention. Further
phenotypic, functional, and genetic analyses of NK cells may provide additional
insights on the pathogenesis of solid organ transplant complications, leading to
the development of biomarkers with potential clinical value.
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