Abstract
Abstract We previously found that adiponectin (APN) suppresses IL-2-induced natural killer (NK) cell activation by down-regulating IFN-γ-inducible tumor necrosis factor-related apoptosis-inducing ligand and Fas ligand expression. Even though APN’s anti-tumor function has been reported in several solid tumors, with few controversial results, no lymphoma studies have been conducted. In this study, we assessed APN’s role in the function of immune cells, including NK cells, cytotoxic T-lymphocytes (CTL), and myeloid-derived suppressor cells (MDSC), using EL4 and B16F10-bearing C57BL/6J based APN-knockout (APNKO) mice. We observed attenuated EL4 growth in APNKO mice. Increased numbers of splenic NK cells were found under naive conditions and splenic CTLs under EL4-challenged conditions. Splenic NK cells in APNKO mice showed enhanced cytotoxicity, with and without IL-2 stimulation. In addition, decreased MDSC accumulation was found in EL4-bearing APNKO mice. Enforced MHC class I (MHC I) expression in B16F10 led to attenuated growth in APNKO mice. Thus, our results suggest that EL4 regression in APNKO mice is due to not only enhanced anti-tumor immune system but also to high level expression of MHC I.
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