Cutting edge: Origins, recruitment, and regulation of CD11c+ cells in inflamed islets of autoimmune diabetes mice

Joanna E. Klementowicz, Ashley E. Mahne, Allyson Spence, Vinh Nguyen, Ansuman T. Satpathy, Kenneth M. Murphy, Qizhi Tang

Research output: Contribution to journalArticlepeer-review

13 Scopus citations

Abstract

In NOD mice, CD11c+ cells increase greatly with islet inflammation and contribute to autoimmune destruction of pancreatic b 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 Agspecific 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.

Original languageEnglish
Pages (from-to)27-32
Number of pages6
JournalJournal of Immunology
Volume199
Issue number1
DOIs
StatePublished - Jul 1 2017

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