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Arginine depletion as a mechanism for the immune privilege of corneal allografts

Arginine depletion as a mechanism for the immune privilege of corneal allografts
Arginine depletion as a mechanism for the immune privilege of corneal allografts

The cornea is an immune privileged tissue. Since arginase has been found to modulate T-cell function by depleting arginine, we investigated the expression of arginase in the cornea and its possible role in immune privilege using a murine transplant model. We found that both the endothelium and epithelium of murine corneas express functional arginase I, capable of down-regulating T-cell proliferation in an in vitro culture system. The administration of the specific arginase inhibitor N-hydroxy-nor-L-Arg to recipient mice resulted in an accelerated rejection of allogeneic C57BL/6 (B6) corneal grafts. In contrast, in vivo blockade of arginase activity had no effect in altering the course of rejection of primary skin grafts that express little, if any, arginase. In addition, the inhibition of arginase did not alter systemic T-cell proliferation. These data show that arginase is functional in the cornea and contributes to the immune privilege of the eye, and that modulation of arginase contributes to graft survival.

Animals, Arginase/antagonists & inhibitors, Arginine/administration & dosage, CD4-Positive T-Lymphocytes/metabolism, Cell Proliferation/drug effects, Cells, Cultured, Cornea/immunology, Corneal Transplantation, Endothelium, Corneal/immunology, Epithelium, Corneal/immunology, Graft Survival, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Polymerase Chain Reaction, Skin Transplantation, Transplantation, Homologous
0014-2980
2997-3005
Fu, Hongmei
b170bb68-1a5e-410f-bbb4-127ee6e5ef63
Khan, Adnan
97374057-d7e7-4849-ac94-c125ba1cc360
Coe, David
3014ec98-ba69-4aea-a61e-215ef01ce8be
Zaher, Sarah
70c5f37f-f584-4edc-9bc8-ee92d1073a33
Chai, Jian-Guo
1743a74d-b595-40c9-a787-a21d486d51a5
Kropf, Pascale
631faa24-4df8-4ab4-b8a6-0470e0ba1033
Müller, Ingrid
0320bc7b-1581-41ec-9ed3-bb7a13812d83
Larkin, Daniel F.P.
bd692846-4d50-48bd-a359-8b8bb02f58e7
George, Andrew J.T.
6b2bc9a6-79eb-4f70-a652-f3f1470e4b86
Fu, Hongmei
b170bb68-1a5e-410f-bbb4-127ee6e5ef63
Khan, Adnan
97374057-d7e7-4849-ac94-c125ba1cc360
Coe, David
3014ec98-ba69-4aea-a61e-215ef01ce8be
Zaher, Sarah
70c5f37f-f584-4edc-9bc8-ee92d1073a33
Chai, Jian-Guo
1743a74d-b595-40c9-a787-a21d486d51a5
Kropf, Pascale
631faa24-4df8-4ab4-b8a6-0470e0ba1033
Müller, Ingrid
0320bc7b-1581-41ec-9ed3-bb7a13812d83
Larkin, Daniel F.P.
bd692846-4d50-48bd-a359-8b8bb02f58e7
George, Andrew J.T.
6b2bc9a6-79eb-4f70-a652-f3f1470e4b86

Fu, Hongmei, Khan, Adnan, Coe, David, Zaher, Sarah, Chai, Jian-Guo, Kropf, Pascale, Müller, Ingrid, Larkin, Daniel F.P. and George, Andrew J.T. (2011) Arginine depletion as a mechanism for the immune privilege of corneal allografts. European Journal of Immunology, 41 (10), 2997-3005. (doi:10.1002/eji.201141683).

Record type: Article

Abstract

The cornea is an immune privileged tissue. Since arginase has been found to modulate T-cell function by depleting arginine, we investigated the expression of arginase in the cornea and its possible role in immune privilege using a murine transplant model. We found that both the endothelium and epithelium of murine corneas express functional arginase I, capable of down-regulating T-cell proliferation in an in vitro culture system. The administration of the specific arginase inhibitor N-hydroxy-nor-L-Arg to recipient mice resulted in an accelerated rejection of allogeneic C57BL/6 (B6) corneal grafts. In contrast, in vivo blockade of arginase activity had no effect in altering the course of rejection of primary skin grafts that express little, if any, arginase. In addition, the inhibition of arginase did not alter systemic T-cell proliferation. These data show that arginase is functional in the cornea and contributes to the immune privilege of the eye, and that modulation of arginase contributes to graft survival.

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More information

Accepted/In Press date: 20 July 2011
e-pub ahead of print date: 29 July 2011
Published date: October 2011
Keywords: Animals, Arginase/antagonists & inhibitors, Arginine/administration & dosage, CD4-Positive T-Lymphocytes/metabolism, Cell Proliferation/drug effects, Cells, Cultured, Cornea/immunology, Corneal Transplantation, Endothelium, Corneal/immunology, Epithelium, Corneal/immunology, Graft Survival, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Polymerase Chain Reaction, Skin Transplantation, Transplantation, Homologous

Identifiers

Local EPrints ID: 432528
URI: http://eprints.soton.ac.uk/id/eprint/432528
ISSN: 0014-2980
PURE UUID: a343812b-2aaf-4421-9d85-ed430bbcc99f
ORCID for Adnan Khan: ORCID iD orcid.org/0000-0001-8153-8002

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Date deposited: 17 Jul 2019 16:30
Last modified: 16 Mar 2024 04:40

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Contributors

Author: Hongmei Fu
Author: Adnan Khan ORCID iD
Author: David Coe
Author: Sarah Zaher
Author: Jian-Guo Chai
Author: Pascale Kropf
Author: Ingrid Müller
Author: Daniel F.P. Larkin
Author: Andrew J.T. George

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