title: Adiponectin deficiency suppresses lymphoma growth in mice by modulating NK cells, CD8 T cells, and myeloid-derived suppressor cells.
abstract: Previously, we found that adiponectin (APN) suppresses IL-2-induced NK cell activation by downregulating the expression of the IFN-γ-inducible TNF-related apoptosis-inducing ligand and Fas ligand. Although the antitumor function of APN has been reported in several types of solid tumors, with few controversial results, no lymphoma studies have been conducted. In this study, we assessed the role of APN in immune cell function, including NK cells, CTLs, and myeloid-derived suppressor cells, in EL4 and B16F10 tumor-bearing APN knockout (KO) mice. We observed attenuated EL4 growth in the APNKO mice. Increased numbers of splenic NK cells and splenic CTLs were identified under naive conditions and EL4-challenged conditions, respectively. In APNKO mice, splenic NK cells showed enhanced cytotoxicity with and without IL-2 stimulation. Additionally, there were decreased levels of myeloid-derived suppressor cell accumulation in the EL4-bearing APNKO mice. Enforced MHC class I expression on B16F10 cells led to attenuated growth of these tumors in APNKO mice. Thus, our results suggest that EL4 regression in APNKO mice is not only due to an enhanced antitumor immune response but also to a high level of MHC class I expression.
authors.affiliation: Research Center for Women's Disease, Department of Life Science, Sookmyung Women's University, Seoul 140-742, Republic of Korea.
authors.forename: Sora
authors.initials: S
authors.lastname: Han
authors.forename: Ae Lee
authors.initials: AL
authors.lastname: Jeong
authors.forename: Sunyi
authors.initials: S
authors.lastname: Lee
authors.forename: Jeong Su
authors.initials: JS
authors.lastname: Park
authors.forename: Kwang Dong
authors.initials: KD
authors.lastname: Kim
authors.forename: Inpyo
authors.initials: I
authors.lastname: Choi
authors.forename: Suk Ran
authors.initials: SR
authors.lastname: Yoon
authors.forename: Myung Sok
authors.initials: MS
authors.lastname: Lee
authors.forename: Jong-Seok
authors.initials: JS
authors.lastname: Lim
authors.forename: Seung Hyun
authors.initials: SH
authors.lastname: Han
authors.forename: Do Young
authors.initials: DY
authors.lastname: Yoon
authors.forename: Young
authors.initials: Y
authors.lastname: Yang
mesh_terms: D052242:Adiponectin / Q000172:deficiency* / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D000818:Animals; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology* / Q000378:metabolism; D016466:CHO Cells; D002454:Cell Differentiation / Q000235:genetics; D045744:Cell Line, Tumor; D006224:Cricetinae; D005805:Genes, MHC Class I; D016179:Granulocyte Colony-Stimulating Factor / Q000235:genetics / Q000378:metabolism; D007376:Interleukin-2 / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D007694:Killer Cells, Natural / Q000276:immunology* / Q000378:metabolism; D008223:Lymphoma / Q000235:genetics / Q000276:immunology* / Q000378:metabolism / Q000473:pathology*; D008297:Male; D008546:Melanoma, Experimental / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D008661:Metabolism, Inborn Errors / Q000235:genetics / Q000276:immunology* / Q000378:metabolism* / Q000473:pathology; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D022423:Myeloid Cells / Q000276:immunology* / Q000378:metabolism; D055650:NK Cell Lectin-Like Receptor Subfamily A / Q000235:genetics / Q000378:metabolism; D013154:Spleen / Q000378:metabolism; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology / Q000378:metabolism
chemical_list: D052242:Adiponectin; C499919:Adipoq protein, mouse; D007376:Interleukin-2; C527092:Klra4 protein, mouse; D055650:NK Cell Lectin-Like Receptor Subfamily A; D016179:Granulocyte Colony-Stimulating Factor