Neural precursor cells inhibit multiple inflammatory signals

Nina Fainstein, Ilan Vaknin, Ofira Einstein, Philip Zisman, S. Z.Ben Sasson, Michal Baniyash, Tamir Ben-Hur*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

66 Scopus citations

Abstract

Intravenous neural precursor cell (NPCs) injection attenuates experimental autoimmune encephalomyelitis by reducing autoreactive T cell encephalitogenicity in lymph nodes in vivo. Here we examined NPC-lymphocyte interactions in vitro. NPCs inhibited the induction of T cell activation marker IL-2-Receptor α, ICOS, PD-1 and CTLA-4 and inhibited T cell proliferation. NPCs inhibited T cell activation and proliferation in response to Concavalin-A and to anti-CD3/anti-CD28, which are T cell receptor (TCR)-mediated stimuli, but not in response to phorbol myristate acetate/ionomycin, a TCR-independent stimulus. The suppressive effect was not mediated via downregulation of CD3ε or induction of apoptosis. We next examined NPCs effects on inflammatory-cytokine signaling. NPCs impaired IL-2-mediated phosphorylation of JAK3 in lymphocytes, and inhibited IL-6 mediated proliferation of B9 murine hybridoma cells. In conclusion, NPCs ameliorate TCR-mediated T cell activation and inhibit inflammatory cytokines' signaling in immune cells. These findings may underlie the broad anti-inflammatory effects of NPCs in vivo.

Original languageAmerican English
Pages (from-to)335-341
Number of pages7
JournalMolecular and Cellular Neuroscience
Volume39
Issue number3
DOIs
StatePublished - 29 Oct 2008

Bibliographical note

Funding Information:
This work was supported by The Israel Science Foundation (grant 140/05) and The Lena P. Harvey Endowment Fund.

Keywords

  • Inflammatory cytokines
  • Neural precursor cells
  • T cell

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