TLR5-deficiency controls dendritic cell subset development in an autoimmune diabetes-susceptible model.

ABSTRACT:

Introduction

The incidence of the autoimmune disease, type 1 diabetes (T1D), has been increasing worldwide and recent studies have shown that the gut microbiota are associated with modulating susceptibility to T1D. Toll-like receptor 5 (TLR5) recognizes bacterial flagellin and is widely expressed on many cells, including dendritic cells (DCs), which are potent antigen-presenting cells (APCs). TLR5 modulates susceptibility to obesity and alters metabolism through gut microbiota; however, little is known about the role TLR5 plays in autoimmunity, especially in T1D.

Methods

To fill this knowledge gap, we generated a TLR5-deficient non-obese diabetic (NOD) mouse, an animal model of human T1D, for study.

Results

We found that TLR5-deficiency led to a reduction in CD11c

SUBMITTER: Pearson JA 

PROVIDER: S-EPMC10935730 | biostudies-literature | 2024

REPOSITORIES: biostudies-literature