AI Article Synopsis

  • The 802-2 peptide, derived from the human CD4 protein, can interfere with CD4(+) T cell activation in both humans and mice.
  • When tested in mice with experimental allergic encephalomyelitis (EAE), 802-2 significantly lessened disease severity whether given before or after symptoms appeared.
  • Mice treated with 802-2 showed reduced immune responses to a specific antigen but could still respond to other antigens, highlighting its potential as a therapy to limit harmful CD4(+) T cell activity in neuroinflammatory diseases.

Article Abstract

The 802-2 peptide, designed from the conserved D1-CC' loop region of human CD4, can disrupt CD4(+) T cell activation in both human and murine systems. Here, 802-2 was investigated for efficacy in acute murine experimental allergic encephalomyelitis (EAE) models, and was found to significantly reduce the severity of disease when administered either before or after the onset of symptoms. 802-2 treatment during PLP139-151 induction of EAE rendered the mice more resistant to subsequent rechallenge with antigen, and was also efficacious when initially administered during a secondary EAE response. T cells from 802-2-treated mice proliferated poorly to in vitro restimulation with PLP139-151 and exhibited decreased frequencies of IL-2, IL-4, and IFN-gamma producing cells, but were still able to respond to third-party antigens. These combined results suggest the potential therapeutic value of 802-2 for inhibition of CD4(+) T cell neuroimmunological responses.

Download full-text PDF

Source
http://dx.doi.org/10.1016/s0165-5728(00)00393-3DOI Listing

Publication Analysis

Top Keywords

human cd4
8
loop region
8
murine experimental
8
experimental allergic
8
allergic encephalomyelitis
8
cd4+ cell
8
cyclic heptapeptide
4
heptapeptide based
4
based human
4
cd4 domain
4

Similar Publications

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!