Fig. 4.

A hypothetical mechanism how NKEF-A and -B (Prx1 and 2) could enhance NK cell activity. Prx1 has stronger NK cell enhancing activity than Prx2.⁽¹⁷⁾ Prx1 and presumably Prx2 bind TLR4 expressed on NK cells inducing activation of NK cells through production of chemokine and IFN-γ.⁽⁸⁰⁾ It is also possible that Prx1 binds to MIF and inhibits its activity. MIF can be released from target cells and is contained in serum, resulting in down-regulation of NKG2D expression,⁽⁸¹⁾ a receptor important for perforin-mediated cytolytic response. This effect might be restricted to Prx1 since binding of Prx2 with MIF is not shown.