Gemcitabine directly inhibits effector CD4 T cell activation and prevents experimental autoimmune encephalomyelitis

Justin D. Glenn, Patrick Xue, Katharine A. Whartenby

Research output: Contribution to journalArticlepeer-review

Abstract

Pro-inflammatory T cells are critical to the pathogenesis of multiple sclerosis (MS). We investigated the potential for the anti-proliferative, pro-apoptotic drug gemcitabine to affect development of MS-relevant effector TH1, TH17, and Treg cells. Gemcitabine directly suppressed proliferation, activation, and induced apoptosis of all effector subsets in subtype and dose-dependent fashion. This drug also prevented development of disease in the MS model experimental autoimmune encephalomyelitis (EAE) and significantly reduced the abundance of TH1 and TH17 cells. Our results indicate that pathogenic CD4+ T cells may be viable targets by gemcitabine for therapeutic benefit in MS.

Original languageEnglish (US)
Pages (from-to)7-16
Number of pages10
JournalJournal of Neuroimmunology
Volume316
DOIs
StatePublished - Mar 15 2018
Externally publishedYes

Keywords

  • Experimental autoimmune encephalomyelitis
  • Multiple sclerosis
  • Neuro-inflammation
  • T cell

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Neurology
  • Clinical Neurology

Fingerprint

Dive into the research topics of 'Gemcitabine directly inhibits effector CD4 T cell activation and prevents experimental autoimmune encephalomyelitis'. Together they form a unique fingerprint.

Cite this