| First Author | Kobayashi S | Year | 2022 |
| Journal | Int J Cancer | Volume | 150 |
| Issue | 1 | Pages | 152-163 |
| PubMed ID | 34449874 | Mgi Jnum | J:322120 |
| Mgi Id | MGI:6833904 | Doi | 10.1002/ijc.33777 |
| Citation | Kobayashi S, et al. (2022) Fatty acid-binding protein 5 limits the generation of Foxp3(+) regulatory T cells through regulating plasmacytoid dendritic cell function in the tumor microenvironment. Int J Cancer 150(1):152-163 |
| abstractText | Plasmacytoid dendritic cells (pDCs) promote viral elimination by producing large amounts of Type I interferon. Recent studies have shown that pDCs regulate the pathogenesis of diverse inflammatory diseases, such as cancer. Fatty acid-binding protein 5 (FABP5) is a cellular chaperone of long-chain fatty acids that induce biological responses. Although the effects of FABP-mediated lipid metabolism are well studied in various immune cells, its role in pDCs remains unclear. This study, which compares wild-type and Fabp5(-/-) mice, provides the first evidence that FABP5-mediated lipid metabolism regulates the commitment of pDCs to inflammatory vs tolerogenic gene expression patterns in the tumor microenvironment and in response to toll-like receptor stimulation. Additionally, we demonstrated that FABP5 deficiency in pDCs affects the surrounding cellular environment, and that FABP5 expression in pDCs supports the appropriate generation of regulatory T cells (Tregs). Collectively, our findings reveal that pDC FABP5 acts as an important regulator of tumor immunity by controlling lipid metabolism. |
