| First Author | Klementowicz JE | Year | 2017 |
| Journal | J Immunol | Volume | 199 |
| Issue | 1 | Pages | 27-32 |
| PubMed ID | 28550204 | Mgi Jnum | J:250651 |
| Mgi Id | MGI:6100316 | Doi | 10.4049/jimmunol.1601062 |
| Citation | Klementowicz JE, et al. (2017) Cutting Edge: Origins, Recruitment, and Regulation of CD11c(+) Cells in Inflamed Islets of Autoimmune Diabetes Mice. J Immunol 199(1):27-32 |
| abstractText | In NOD mice, CD11c(+) cells increase greatly with islet inflammation and contribute to autoimmune destruction of pancreatic beta cells. In this study, we investigated their origin and mechanism of recruitment. CD11c(+) cells in inflamed islets resembled classical dendritic cells based on their transcriptional profile. However, the majority of these cells were not from the Zbtb46-dependent dendritic-cell lineage. Instead, monocyte precursors could give rise to CD11c(+) cells in inflamed islets. Chemokines Ccl5 and Ccl8 were persistently elevated in inflamed islets and the influx of CD11c(+) cells was partially dependent on their receptor Ccr5. Treatment with islet Ag-specific regulatory T cells led to a marked decrease of Ccl5 and Ccl8, and a reduction of monocyte recruitment. These results implicate a monocytic origin of CD11c(+) cells in inflamed islets and suggest that therapeutic regulatory T cells directly or indirectly regulate their influx by altering the chemotactic milieu in the islets. |
