| Literature DB >> 31343073 |
A M Sandor1,2, J Jacobelli1,2, R S Friedman1,2.
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.Entities:
Keywords: adhesion molecules; autoimmunity; cell trafficking; chemokines; diabetes
Mesh:
Year: 2019 PMID: 31343073 PMCID: PMC6857188 DOI: 10.1111/cei.13353
Source DB: PubMed Journal: Clin Exp Immunol ISSN: 0009-9104 Impact factor: 4.330