A new study published in March 2013 issue of the Journal of Immunology identifies a new immunomodulatory effect of adiponectin (APN) – its ability to activate DCs through PLCγ/JNK/NF-κB-signaling pathways and release of proinflammatory cytokines, and to potentiate Th1 and Th17 immune responses.
Adiponectin, the most abundant adipokine, is known for its insulin-sensitizing effects, is an indicator of the onset of some cardiovascular diseases, and is highly expressed in inflamed tissues from patients with rheumatoid arthritis and inflammatory bowel disease.
Increased concentrations of APN are reported in chronic inflammatory diseases, such as inflammatory bowel disease, osteoarthritis, and rheumatoid arthritis.
In the Journal of Immunology study, Mi Jung and colleagues from the School of Life Sciences and Biotechnology, Korea University, Seoul, Republic of Korea, demonstrate that APN is able to activate dendritic cells through enhancement of the co-stimulatory molecules and MHC class II, and release of proinflammatory cytokines, thus leading to Th1 and Th17 polarization and phenotypes.
Through this mechanism, APN may contribute to Th1- and Th17-mediated inflammatory and/or autoimmune diseases. Thus, increased levels of APN released locally at the inflammatory site, such as in established colitis and arthritis, may contribute to the perpetuation of inflammation, exacerbating the disease process.
Source: J Immunol, 2012 Mar 15; 188:2592. doi: 10.4049/jimmunol.1102588. Epub 2012 Feb 15.