In addition, there was no association between specific NK phenotype, effector function, KIR mismatching, or circulating [CD56.sup.+] cell number postinfusion and response.
Five patients achieved a morphologic CR, including 75% of those with KIR mismatch versus 13% of those without.
Interestingly, no differences in toxicities or survival endpoints were noted based on KIR mismatching or donor activation of KIR.
This study divided patients into 2 cohorts: a phase I dose escalation (15 patients with KIR mismatch) and a phase II expansion (6 CML patients, KIR mismatch not required).
However, the effect of Juzen-taiho-to alone or with cytokines on the expression of KIRs:CD158a/b, which is involved in NK cell function, has not been studied.
The upregulation of KIRs expression does not directly induce a decrease of NK cytolytic activity, namely, when activated NK cells lyse neoplastic cells, they must specifically distinguish non-MHC class I cells from normal cells under the delicate balance required for specific killing.
In contrast, IL-2 also upregulates the expression of KIRs on the CD16 non-expressing cells (Kogure et al., 2001).
IL-2 upregulates the expression of KIRs (Kogure et al., 1999).
To explore whether HLA ligands for KIR could influence the onset age of HBVrelated HCC, we grouped HLA alleles according to KIR ligand as Bw4, Bw4T, Bw4I, HLA-C1, and HLA-C2.
In this study, we examined the KIR and HLA genetic background in 171 male patients.
In our previous case-control study, several KIR and HLA variants, including HLA-C1C1, HLA-Bw4-80I, and KIR2DS4(f)/(d), were identified as the risk factors for HCC development in the patients with HBV infection.