| First Author | Rothe K | Year | 2017 |
| Journal | Eur J Immunol | Volume | 47 |
| Issue | 9 | Pages | 1457-1467 |
| PubMed ID | 28664612 | Mgi Jnum | J:246254 |
| Mgi Id | MGI:5924366 | Doi | 10.1002/eji.201646747 |
| Citation | Rothe K, et al. (2017) Autoimmune arthritis induces paired immunoglobulin-like receptor B expression on CD4+ T cells from SKG mice. Eur J Immunol 47(9):1457-1467 |
| abstractText | The chronic, destructive autoimmune arthritis in SKG mice, which closely resembles human rheumatoid arthritis, is the result of self-reactive T cells escaping thymic deletion. Since the inhibitory receptor LIR-1 is up-regulated on auto-reactive T cells in human rheumatoid arthritis, the role of its murine ortholog PIR-B was investigated. Peripheral CD4+ T cells from SKG mice were found to frequently express PIR-B, and this population produces more frequently IL-17 upon in vitro stimulation compared to PIR-B- cells. A much larger fraction of PIR-B+ T cells, however, was found to secret no IL-17, but IFN-gamma. With regards to the clinical course of the disease, high frequencies of PIR-B+ CD4+ T cells were found to be associated with a milder course of arthritis, suggesting that the net effect of PIR-B expression is suppression of autoreactive T cells. Our results indicate that overexpression of PIR-B on IL-17-producing SKG CD4+ T cells might represent an effective counter-regulatory mechanism against the destructive potential of those cells. More importantly, a major population of PIR-B+ T cells in SKG mice appears to play an inhibitory role by way of their IFN-gamma production, since high frequencies of those cells ameliorate the disease. |
