Ocular production of interferon-gamma and lack of major histocompatibility complex molecules induce immunological changes in the intraocular environment.

K. D. Geiger, Nora E Sarvetnick

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

The intraocular immune privilege includes the absence of delayed-type hypersensitivity (DTH) to intraocularly presented antigens. To study the role of major histocompatibility complex (MHC) molecules in relation to the activity of the proinflammatory cytokine interferon-gamma (IFN-gamma) in the maintenance of the intraocular immune privilege, we tested DTH to intraocularly presented antigens in MHC class I- or class II-deficient mice and in transgenic mice with production of IFN-gamma in the retina (rho-gamma). MHC class I- and class II-deficient mice and rho gamma mice with or without additional MHC deficiency developed hypersensitivity to intraocularly presented antigens and increased ocular pathology, whereas control animals did not. The abrogation of the intraocular immune privilege by IFN-gamma was independent of MHC expression and was probably due to disturbance of the blood-retina barrier. The sole lack of MHC class I or II expression produced similar effects, confirming the importance of IFN-gamma and MHC molecules for the development of uveitis.

Original languageEnglish (US)
Pages (from-to)309-314
Number of pages6
JournalGerman journal of ophthalmology
Volume5
Issue number6
StatePublished - Jan 1 1996
Externally publishedYes

Fingerprint

Major Histocompatibility Complex
Interferon-gamma
Delayed Hypersensitivity
Antigens
Retina
Uveitis
Transgenic Mice
Hypersensitivity
Maintenance
Pathology
Cytokines

ASJC Scopus subject areas

  • Medicine(all)

Cite this

@article{930fc351b6b4406586101654ea3210f1,
title = "Ocular production of interferon-gamma and lack of major histocompatibility complex molecules induce immunological changes in the intraocular environment.",
abstract = "The intraocular immune privilege includes the absence of delayed-type hypersensitivity (DTH) to intraocularly presented antigens. To study the role of major histocompatibility complex (MHC) molecules in relation to the activity of the proinflammatory cytokine interferon-gamma (IFN-gamma) in the maintenance of the intraocular immune privilege, we tested DTH to intraocularly presented antigens in MHC class I- or class II-deficient mice and in transgenic mice with production of IFN-gamma in the retina (rho-gamma). MHC class I- and class II-deficient mice and rho gamma mice with or without additional MHC deficiency developed hypersensitivity to intraocularly presented antigens and increased ocular pathology, whereas control animals did not. The abrogation of the intraocular immune privilege by IFN-gamma was independent of MHC expression and was probably due to disturbance of the blood-retina barrier. The sole lack of MHC class I or II expression produced similar effects, confirming the importance of IFN-gamma and MHC molecules for the development of uveitis.",
author = "Geiger, {K. D.} and Sarvetnick, {Nora E}",
year = "1996",
month = "1",
day = "1",
language = "English (US)",
volume = "5",
pages = "309--314",
journal = "German journal of ophthalmology",
issn = "0941-2921",
publisher = "Springer Verlag",
number = "6",

}

TY - JOUR

T1 - Ocular production of interferon-gamma and lack of major histocompatibility complex molecules induce immunological changes in the intraocular environment.

AU - Geiger, K. D.

AU - Sarvetnick, Nora E

PY - 1996/1/1

Y1 - 1996/1/1

N2 - The intraocular immune privilege includes the absence of delayed-type hypersensitivity (DTH) to intraocularly presented antigens. To study the role of major histocompatibility complex (MHC) molecules in relation to the activity of the proinflammatory cytokine interferon-gamma (IFN-gamma) in the maintenance of the intraocular immune privilege, we tested DTH to intraocularly presented antigens in MHC class I- or class II-deficient mice and in transgenic mice with production of IFN-gamma in the retina (rho-gamma). MHC class I- and class II-deficient mice and rho gamma mice with or without additional MHC deficiency developed hypersensitivity to intraocularly presented antigens and increased ocular pathology, whereas control animals did not. The abrogation of the intraocular immune privilege by IFN-gamma was independent of MHC expression and was probably due to disturbance of the blood-retina barrier. The sole lack of MHC class I or II expression produced similar effects, confirming the importance of IFN-gamma and MHC molecules for the development of uveitis.

AB - The intraocular immune privilege includes the absence of delayed-type hypersensitivity (DTH) to intraocularly presented antigens. To study the role of major histocompatibility complex (MHC) molecules in relation to the activity of the proinflammatory cytokine interferon-gamma (IFN-gamma) in the maintenance of the intraocular immune privilege, we tested DTH to intraocularly presented antigens in MHC class I- or class II-deficient mice and in transgenic mice with production of IFN-gamma in the retina (rho-gamma). MHC class I- and class II-deficient mice and rho gamma mice with or without additional MHC deficiency developed hypersensitivity to intraocularly presented antigens and increased ocular pathology, whereas control animals did not. The abrogation of the intraocular immune privilege by IFN-gamma was independent of MHC expression and was probably due to disturbance of the blood-retina barrier. The sole lack of MHC class I or II expression produced similar effects, confirming the importance of IFN-gamma and MHC molecules for the development of uveitis.

UR - http://www.scopus.com/inward/record.url?scp=0030274535&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030274535&partnerID=8YFLogxK

M3 - Article

VL - 5

SP - 309

EP - 314

JO - German journal of ophthalmology

JF - German journal of ophthalmology

SN - 0941-2921

IS - 6

ER -