Anterior chamber-associated immune deviation promotes corneal allograft survival

Jerry Y. Niederkorn, Jessamee Mellon

Research output: Contribution to journalArticle

105 Citations (Scopus)

Abstract

Purpose. To determine whether anterior chamber-associated immune deviation (ACAID) promotes corneal allograft survival. Methods. CB6F1 mice were grafted with orthotopic corneal transplants from C3H donors (mismatch at the entire major histocompatibility complex plus multiple major histocompatibility loci) and from NZB donors (mismatch only at multiple minor histocompatibility loci). ACAID was induced by priming in the anterior chamber (AC) with either Ia+ spleen cells, Ia+ spleen cells, corneal endothelial cells, or corneal epithelial cells from corneal allograft donors before orthotopic transplantation. The role of ACAID in promoting corneal allograft survival was examined by determining the fate of corneal allografts in splenectomized and eusplenic mice. Results. Anterior chamber priming produced a modest enhancement of the survival of fully allogeneic C3H corneal allografts. By contrast, AC priming with Ia- NZB spleen cells or NZB corneal endothelial cells results in the permanent acceptance of NZB corneal grafts in 60% and 90% of the CB6F1 hosts, respectively. Abolition of ACAID by splenectomy resulted in a sharp increase in the incidence of graft rejection in donor-host combinations involving multiple minor histocompatibility disparity. Conclusions. Anterior chamber priming with alloantigens promotes corneal allografts survival in nonimmune and preimmune hosts. Disruption of the camero-splenic axis prevents the induction of ACAID and greatly increases the risk for corneal allograft rejection.

Original languageEnglish (US)
Pages (from-to)2700-2707
Number of pages8
JournalInvestigative Ophthalmology and Visual Science
Volume37
Issue number13
StatePublished - Dec 1996

Fingerprint

Anterior Chamber
Allografts
Histocompatibility
Spleen
Minor Histocompatibility Loci
Endothelial Cells
Transplants
Isoantigens
Graft Rejection
Splenectomy
Major Histocompatibility Complex
Transplantation
Epithelial Cells
Incidence

Keywords

  • anterior chamber-associated immune deviation (ACAID)
  • corneal allografts
  • immune privilege
  • keratoplasty

ASJC Scopus subject areas

  • Ophthalmology

Cite this

Anterior chamber-associated immune deviation promotes corneal allograft survival. / Niederkorn, Jerry Y.; Mellon, Jessamee.

In: Investigative Ophthalmology and Visual Science, Vol. 37, No. 13, 12.1996, p. 2700-2707.

Research output: Contribution to journalArticle

@article{f39e5b3513f74ea08f62a392a044bbf1,
title = "Anterior chamber-associated immune deviation promotes corneal allograft survival",
abstract = "Purpose. To determine whether anterior chamber-associated immune deviation (ACAID) promotes corneal allograft survival. Methods. CB6F1 mice were grafted with orthotopic corneal transplants from C3H donors (mismatch at the entire major histocompatibility complex plus multiple major histocompatibility loci) and from NZB donors (mismatch only at multiple minor histocompatibility loci). ACAID was induced by priming in the anterior chamber (AC) with either Ia+ spleen cells, Ia+ spleen cells, corneal endothelial cells, or corneal epithelial cells from corneal allograft donors before orthotopic transplantation. The role of ACAID in promoting corneal allograft survival was examined by determining the fate of corneal allografts in splenectomized and eusplenic mice. Results. Anterior chamber priming produced a modest enhancement of the survival of fully allogeneic C3H corneal allografts. By contrast, AC priming with Ia- NZB spleen cells or NZB corneal endothelial cells results in the permanent acceptance of NZB corneal grafts in 60{\%} and 90{\%} of the CB6F1 hosts, respectively. Abolition of ACAID by splenectomy resulted in a sharp increase in the incidence of graft rejection in donor-host combinations involving multiple minor histocompatibility disparity. Conclusions. Anterior chamber priming with alloantigens promotes corneal allografts survival in nonimmune and preimmune hosts. Disruption of the camero-splenic axis prevents the induction of ACAID and greatly increases the risk for corneal allograft rejection.",
keywords = "anterior chamber-associated immune deviation (ACAID), corneal allografts, immune privilege, keratoplasty",
author = "Niederkorn, {Jerry Y.} and Jessamee Mellon",
year = "1996",
month = "12",
language = "English (US)",
volume = "37",
pages = "2700--2707",
journal = "Investigative Ophthalmology and Visual Science",
issn = "0146-0404",
publisher = "Association for Research in Vision and Ophthalmology Inc.",
number = "13",

}

TY - JOUR

T1 - Anterior chamber-associated immune deviation promotes corneal allograft survival

AU - Niederkorn, Jerry Y.

AU - Mellon, Jessamee

PY - 1996/12

Y1 - 1996/12

N2 - Purpose. To determine whether anterior chamber-associated immune deviation (ACAID) promotes corneal allograft survival. Methods. CB6F1 mice were grafted with orthotopic corneal transplants from C3H donors (mismatch at the entire major histocompatibility complex plus multiple major histocompatibility loci) and from NZB donors (mismatch only at multiple minor histocompatibility loci). ACAID was induced by priming in the anterior chamber (AC) with either Ia+ spleen cells, Ia+ spleen cells, corneal endothelial cells, or corneal epithelial cells from corneal allograft donors before orthotopic transplantation. The role of ACAID in promoting corneal allograft survival was examined by determining the fate of corneal allografts in splenectomized and eusplenic mice. Results. Anterior chamber priming produced a modest enhancement of the survival of fully allogeneic C3H corneal allografts. By contrast, AC priming with Ia- NZB spleen cells or NZB corneal endothelial cells results in the permanent acceptance of NZB corneal grafts in 60% and 90% of the CB6F1 hosts, respectively. Abolition of ACAID by splenectomy resulted in a sharp increase in the incidence of graft rejection in donor-host combinations involving multiple minor histocompatibility disparity. Conclusions. Anterior chamber priming with alloantigens promotes corneal allografts survival in nonimmune and preimmune hosts. Disruption of the camero-splenic axis prevents the induction of ACAID and greatly increases the risk for corneal allograft rejection.

AB - Purpose. To determine whether anterior chamber-associated immune deviation (ACAID) promotes corneal allograft survival. Methods. CB6F1 mice were grafted with orthotopic corneal transplants from C3H donors (mismatch at the entire major histocompatibility complex plus multiple major histocompatibility loci) and from NZB donors (mismatch only at multiple minor histocompatibility loci). ACAID was induced by priming in the anterior chamber (AC) with either Ia+ spleen cells, Ia+ spleen cells, corneal endothelial cells, or corneal epithelial cells from corneal allograft donors before orthotopic transplantation. The role of ACAID in promoting corneal allograft survival was examined by determining the fate of corneal allografts in splenectomized and eusplenic mice. Results. Anterior chamber priming produced a modest enhancement of the survival of fully allogeneic C3H corneal allografts. By contrast, AC priming with Ia- NZB spleen cells or NZB corneal endothelial cells results in the permanent acceptance of NZB corneal grafts in 60% and 90% of the CB6F1 hosts, respectively. Abolition of ACAID by splenectomy resulted in a sharp increase in the incidence of graft rejection in donor-host combinations involving multiple minor histocompatibility disparity. Conclusions. Anterior chamber priming with alloantigens promotes corneal allografts survival in nonimmune and preimmune hosts. Disruption of the camero-splenic axis prevents the induction of ACAID and greatly increases the risk for corneal allograft rejection.

KW - anterior chamber-associated immune deviation (ACAID)

KW - corneal allografts

KW - immune privilege

KW - keratoplasty

UR - http://www.scopus.com/inward/record.url?scp=0030444098&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030444098&partnerID=8YFLogxK

M3 - Article

VL - 37

SP - 2700

EP - 2707

JO - Investigative Ophthalmology and Visual Science

JF - Investigative Ophthalmology and Visual Science

SN - 0146-0404

IS - 13

ER -