These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Treatment with intact anti-B7-1 mAb during disease remission enhances epitope spreading and exacerbates relapses in R-EAE.
    Author: Vanderlugt CL, Karandikar NJ, Lenschow DJ, Dal Canto MC, Bluestone JA, Miller SD.
    Journal: J Neuroimmunol; 1997 Nov; 79(2):113-8. PubMed ID: 9394783.
    Abstract:
    PLP139-151-induced experimental autoimmune encephalomyelitis in the SJL mouse is a Th1-mediated inflammatory demyelinating disease characterized by a relapsing-remitting clinical course (R-EAE). Clinical relapses are mediated by T cells specific for a non-cross reactive secondary PLP epitope (PLP178-191) induced by epitope spreading. We have previously shown that B7-1 expression is upregulated in SJL mice undergoing R-EAE and in vivo treatment during remission with F(ab) fragments of anti-B7-1 mAb, blocked epitope spreading and disease progression. In contrast, the present study shows that treatment with intact anti-B7-1 mAb exacerbated clinical disease relapses and enhanced CNS demyelination. Anti-B7-1-treated mice showed enhanced in vivo delayed-type hypersensitivity (DTH) to the relapse-associated PLP178-191 epitope and responses to the immunodominant MBP84-104 epitope which are absent in the controls. Thus, ligation of B7-1 by intact mAbs has effects opposite to those of anti-B7-1 F(ab) fragments suggesting that the mAb is directly signaling through B7-1 expressed on T cells and/or APCs.
    [Abstract] [Full Text] [Related] [New Search]