Co-delivery of autoantigen and b7 pathway modulators suppresses experimental autoimmune encephalomyelitis

Laura Northrup, Joshua O. Sestak, Bradley P. Sullivan, Sharadvi Thati, Brittany L. Hartwell, Teruna J. Siahaan, Charlotte M. Vines, Cory Berkland

Research output: Contribution to journalArticlepeer-review

26 Scopus citations


Autoimmune diseases such as multiple sclerosis (MS) are characterized by the breakdown of immune tolerance to autoantigens. Targeting surface receptors on immune cells offers a unique strategy for reprogramming immune responses in autoimmune diseases. The B7 signaling pathway was targeted using adaptations of soluble antigen array (SAgA) technology achieved by covalently linking B7-binding peptides and disease causing autoantigen (proteolipid peptide (PLP)) to hyaluronic acid (HA). We hypothesized that co-delivery of a B7-binding peptide and autoantigen would suppress experimental autoimmune encephalomyelitis (EAE), a murine model of MS. Three independent B7-targeted SAgAs were created containing peptides to either inhibit or potentially stimulate the B7 signaling pathway. Surprisingly, all SAgAs were found to suppress EAE disease symptoms. Altered cytokine expression was observed in primary splenocytes isolated from SAgA-treated mice, indicating that SAgAs with different B7-binding peptides may suppress EAE through different immunological mechanisms. This antigen-specific immunotherapy using SAgAs can successfully suppress EAE through co-delivery of autoantigen and peptides targeting with the B7 signaling pathway.

Original languageEnglish (US)
Pages (from-to)1204-1213
Number of pages10
JournalAAPS Journal
Issue number6
StatePublished - 2014
Externally publishedYes

Bibliographical note

Publisher Copyright:
© 2014 American Association of Pharmaceutical Scientists


  • Antigen-specific immunotherapy
  • B7/CD28:CTLA-4 co-stimulatory pathway
  • Experimental autoimmune encephalomyelitis (EAE)
  • Proteolipid peptide
  • Soluble antigen array


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