protective role of myeloid cells expressing a g-csf receptor polymorphism in an induced model of lupus

Clicks: 309
ID: 201327
2018
Free PDF
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This article has not been analysed, so there is no overall score — reader engagement is measured and shown alongside.
AI Quality Assessment
Not analyzed
Readership in this journal
Emerging

Ranked #131 of 644 articles by views in sudebno-meditsinskaia ekspertiza

Most read Least read

Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 644 in total.

Mint this article as an NFT
Not yet minted

Create a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.

5 SUSD one-off · no wallet required
Sign in to mint
Abstract
The genetic analysis of the lupus-prone NZM2410 mouse has identified a suppressor locus, Sle2c2, which confers resistance to spontaneous lupus in combination with NZM2410 susceptibility loci, or in the chronic graft-versus-host disease (cGVHD) induced model of lupus in the B6.Sle2c2 congenic strain. The candidate gene for Sle2c2, the Csf3r gene encoding the granulocyte colony-stimulating factor receptor (G-CSF-R/CD114), was validated when cGVHD was restored in B6.Sle2c2 mice after treatment with G-CSF. The goal of the project reported herein was to investigate the myeloid cells that confer resistance to cGVHD and to ascertain if the mechanism behind their suppression involves the G-CSF pathway. We showed that despite expressing the highest levels of G-CSF-R, neutrophils play only a modest role in the autoimmune activation induced by cGVHD. We also found reduced expression levels of G-CSF-R on the surface of dendritic cells (DCs) and a differential distribution of DC subsets in response to cGVHD in B6.Sle2c2 versus B6 mice. The CD8α+ DC subset, known for its tolerogenic phenotype, was expanded upon induction of cGVHD in B6.Sle2c2 mice. In addition, the deficiency of CD8α+ DC subset enhanced the severity of cGVHD in B6.Batf3−/− and B6.Sle2c2 mice, confirming their role in suppression of cGVHD. B6.Sle2c2DCs presented lowered activation and antigen presentation abilities and expressed lower levels of genes associated with DC activation and maturation. Exposure to exogenous G-CSF reversed the majority of these phenotypes, suggesting that tolerogenic DCs maintained through a defective G-CSF-R pathway mediated the resistance to cGVHD in B6.Sle2c2 mice.
Reference Key
sivakumar2018frontiersprotective Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Ramya Sivakumar;Georges Abboud;Clayton E. Mathews;Mark A. Atkinson;Laurence Morel
Journal sudebno-meditsinskaia ekspertiza
Year 2018
DOI
10.3389/fimmu.2018.01053
URL
http://journal.frontiersin.org/article/10.3389/fimmu.2018.01053/full
Keywords
neutrophils lupus tolerogenic dendritic cells allergy

Citations

No citations found. To add a citation, contact the admin at info@scimatic.org

Comments

No comments yet. Be the first to comment on this article.