| First Author | Son MH | Year | 2014 |
| Journal | Biochem Biophys Res Commun | Volume | 450 |
| Issue | 1 | Pages | 30-5 |
| PubMed ID | 24882804 | Mgi Jnum | J:221995 |
| Mgi Id | MGI:5643832 | Doi | 10.1016/j.bbrc.2014.05.052 |
| Citation | Ccl5Son MH, et al. (2014) IL-32gamma induces chemotaxis of activated T cells via dendritic cell-derived CCL5. Biochem Biophys Res Commun 450(1):30-5 |
| abstractText | Interleukin (IL)-32 has been associated with a variety of inflammatory diseases including rheumatoid arthritis, vasculitis and Crohn's disease. We have previously reported that IL-32gamma, the IL-32 isoform with the highest biological activity, could act as an immune modulator through regulation of dendritic cell (DC) functions in immune responses. Cell locomotion is crucial for induction of an effective immune response. In this study, we investigated the effect and underlying mechanisms of IL-32gamma on recruitment of T cells. IL-32gamma upregulated the expression of several chemokines including CCL2, CCL4, and CCL5 in the DCs. In particular, IL-32gamma significantly increased CCL5 expression in a dose-dependent manner. Treatment with JNK and NF-kappaB inhibitors suppressed IL-32gamma-induced CCL5 expression in DCs, indicating that IL-32gamma induced CCL5 production through the JNK and NF-kappaB pathways. Furthermore, supernatants from IL-32gamma-treated DCs showed chemotactic activities controlling migration of activated CD4(+) and CD8(+) T cells, and these activities were suppressed by addition of neutralizing anti-CCL5 antibody. These results show that IL-32gamma effectively promotes migration of activated T cells via CCL5 production in DCs. The chemotactic potential of IL-32gamma may explain the pro-inflammatory effects of IL-32 and the pathologic role of IL-32 in immune disorders such as rheumatoid arthritis. |
