Negative and positive co-signaling with anti-BTLA (PJ196) and CTLA4Ig prolongs islet allograft survival

Wayne Truong, Jennifer C. Plester, Wayne W. Hancock, Jonathan Kaye, Shaheed Merani, Kenneth M. Murphy, Theresa L. Murphy, Colin C. Anderson, A. M.James Shapiro

Research output: Contribution to journalArticlepeer-review

26 Scopus citations


The novel coinhibitory receptor B and T lymphocyte attenuator (BTLA) has been implicated in the regulation of autoimmune and may potentially play a role in alloimmune responses. An anti-BTLA monoclonal antibody has been reported to prolong fully major histocompatibility complex-mismatched cardiac allograft survival, and we test the hypothesis that anti-BTLA monoclonal antibody PJ196 may synergize with cytotoxic T lymphocyte antigen-4 immunoglobulin (CTLA4Ig) costimulatory blockade in islet transplantation. We investigated the potential of PJ196, and show that it did not deplete BTLA expressing cells, but it caused down-regulation of BTLA on the surface of lymphocytes and accumulation of cells with regulatory phenotype at the graft site, promoting islet allograft acceptance together with CTLA4Ig. The combination of BTLA coinhibitory modulation and CTLA4Ig costimulatory blockade may be an effective adjunctive strategy for inducing long-term allograft survival.

Original languageEnglish (US)
Pages (from-to)1368-1372
Number of pages5
Issue number10
StatePublished - Nov 2007
Externally publishedYes


  • Coinhibition
  • Costimulatory blockade
  • Islet transplantation
  • Monoclonal antibody
  • Regulatory T cells
  • Tolerance

ASJC Scopus subject areas

  • Transplantation


Dive into the research topics of 'Negative and positive co-signaling with anti-BTLA (PJ196) and CTLA4Ig prolongs islet allograft survival'. Together they form a unique fingerprint.

Cite this