Immune Cell Trafficking to the Islets During Type 1 Diabetes

Clin Exp Immunol. 2019 Dec;198(3):314-325. doi: 10.1111/cei.13353. Epub 2019 Aug 30.

Abstract

Inhibition of immune cell trafficking to the pancreatic islets during type 1 diabetes (T1D) has therapeutic potential, since targeting of T cell and B cell trafficking has been clinically effective in other autoimmune diseases. Trafficking to the islets is characterized by redundancy in adhesion molecule and chemokine usage, which has not enabled effective targeting to date. Additionally, cognate antigen is not consistently required for T cell entry into the islets throughout the progression of disease. However, myeloid cells are required to enable T cell and B cell entry into the islets, and may serve as a convergence point in the pathways controlling this process. In this review we describe current knowledge of the factors that mediate immune cell trafficking to pancreatic islets during T1D progression.

Keywords: adhesion molecules; autoimmunity; cell trafficking; chemokines; diabetes.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • B-Lymphocytes / immunology*
  • Cell Movement / immunology*
  • Diabetes Mellitus, Type 1 / immunology*
  • Diabetes Mellitus, Type 1 / pathology
  • Disease Progression
  • Humans
  • Islets of Langerhans / immunology*
  • Myeloid Cells / immunology
  • Signal Transduction / immunology
  • T-Lymphocytes / immunology*