B1 cells promote pancreas infiltration by autoreactive T cells

Gemma A Ryan, Chun Jing Wang, Jayne L. Chamberlain, Kesley Attridge, Emily M. Schmidt, Rupert Kenefeck, Louise E. Clough, Kyri Dunussi-Joannopoulos, Kai-Michael Toellner, Lucy S.K. Walker

Research output: Contribution to journalArticlepeer-review

Abstract

The entry of autoreactive T cells into the pancreas is a critical checkpoint in the development of autoimmune diabetes. In this study, we identify a role for B1 cells in this process using the DO11 x RIP-mOVA mouse model. In transgenic mice with islet-specific T cells, but no B cells, T cells are primed in the pancreatic lymph node but fail to enter the pancreas. Reconstitution of the B1 cell population by adoptive transfer permits extensive T cell pancreas infiltration. Reconstituted B1 cells traffic to the pancreas and modify expression of adhesion molecules on pancreatic vasculature, notably VCAM-1. Despite substantial pancreas infiltration, islet destruction is minimal unless regulatory T cells are depleted. These data identify a role for B1 cells in permitting circulating islet-specific T cells to access their Ag-bearing tissue and emphasize the existence of multiple checkpoints to regulate autoimmune disease.

Original languageEnglish
Pages (from-to)2800-2807
Number of pages8
JournalJournal of Immunology
Volume185
Issue number5
DOIs
Publication statusPublished - 1 Sep 2010

Keywords

  • adoptive transfer
  • autoimmune diseases
  • B-lymphocyte subsets
  • CD8-positive T-lymphocytes
  • cell movement
  • diabetes mellitus
  • islets of Langerhans
  • lymphocyte depletion
  • ovalbumin
  • vascular cell adhesion molecule-1

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