IL-34-Dependent Intrarenal and Systemic Mechanisms Promote Lupus Nephritis in MRL-Fas^lpr Mice.

ABSTRACT:

Background

In people with SLE and in the MRL-Fas^lpr lupus mouse model, macrophages and autoantibodies are central to lupus nephritis. IL-34 mediates macrophage survival and proliferation, is expressed by tubular epithelial cells (TECs), and binds to the cFMS receptor on macrophages and to a newly identified second receptor, PTPRZ.

Methods

To investigate whether IL-34-dependent intrarenal and systemic mechanisms promote lupus nephritis, we compared lupus nephritis and systemic illness in MRL-Fas^lpr mice expressing IL-34 and IL-34 knockout (KO) MRL-Fas^lpr mice. We also assessed expression of IL-34 and the cFMS and PTPRZ receptors in patients with lupus nephritis.

Results

Intrarenal IL-34 and its two receptors increas

SUBMITTER: Wada Y 

PROVIDER: S-EPMC6362618 | biostudies-literature | 2019 Feb

REPOSITORIES: biostudies-literature