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The Journal of Immunology, Vol 157, Issue 11 4790-4795, Copyright © 1996 by American Association of Immunologists

ARTICLES

Tissue immunogenicity: the role of MHC antigen and the lymphocyte costimulator B7-1

M Coulombe, H Yang, S Guerder, RA Flavell, KJ Lafferty and RG Gill
Barbara Davis Center for Childhood Diabetes/University of Colorado Health Sciences Center, Denver 80262, USA.

Pancreatic islet transplantation represents a potential treatment for insulin-dependent diabetes mellitus. One approach to circumvent the requirement for recipient immune suppression is to reduce or eliminate the immunogenicity of the donor graft prior to transplantation. In this study, we have examined the relative contributions of graft MHC Ag expression and donor-derived costimulatory (CoS) activity to the rejection of islet allografts. Depletion of donor hemopoietic APCs from islet tissue facilitated long-term allograft survival even when donor class I MHC Ag expression was greatly increased by IFN-gamma treatment prior to grafting. Conversely, islet allografts from transgenic mice expressing the CoS molecule B7-1 (CD80) on islet beta cells were acutely rejected even when hemopoietic APCs were eliminated. Thus, B7-1 is sufficient to confer the capacity of islet parenchymal cells to stimulate allorejection. Taken together, these results point towards donor-derived CoS activity as a primary target of intervention therapy to modulate tissue immunogenicity.


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