Major histocompatibility complex class I deficiency prolongs islet allograft survival

Diabetes. 1993 Oct;42(10):1520-7. doi: 10.2337/diab.42.10.1520.

Abstract

Because of islet allograft rejection, nonimmunosuppressed pancreatic islet allotransplantation has been unsuccessful for the treatment of type I diabetes. The role of major histocompatibility complex class I antigen expression on islet allograft survival was evaluated with the use of mice homozygous for a beta 2-microglobulin gene disruption. These mice express little if any functional major histocompatibility complex class I antigen. When these major histocompatibility complex class I-deficient islets were used as donors in an allogenic murine transplantation model, islet allograft survival was markedly prolonged. These results demonstrate a major importance for the alloresponse directed against major histocompatibility complex class I antigen.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Female
  • Gene Expression / genetics
  • Graft Survival* / physiology
  • Histocompatibility Antigens Class I / immunology
  • Histocompatibility Antigens Class I / metabolism
  • Histocompatibility Antigens Class I / physiology*
  • Homozygote
  • Immune System Diseases / metabolism
  • Islets of Langerhans Transplantation* / immunology
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Mutant Strains
  • Models, Biological
  • Transplantation, Homologous
  • beta 2-Microglobulin / genetics
  • beta 2-Microglobulin / physiology

Substances

  • Histocompatibility Antigens Class I
  • beta 2-Microglobulin