Autoimmunity, Autoinflammation, and Infection in Uveitis

John V. Forrester, Lucia Kuffova, Andrew D. Dick

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

Purpose: To review the pathogenesis of uveitis in light of recent advances in our understanding of innate and adaptive immune responses and their regulation. Design: Perspective. Methods: Methods included a review of prevailing views on the pathogenesis of uveitis and an analysis of developments in immunology that impact on its conceptual basis, particularly the concept of immunologic tolerance and its loss in autoimmunity. Importantly, the role of infection in the pathogenesis of uveitis is evaluated. Results: The results comprise a reappraisal of the pathogenesis of anterior vs posterior uveitis in the context of the blood-retinal barrier and its relation to autoimmune, autoinflammatory, and infectious uveitis. Autoimmunity is seen as a possible cause of certain forms of uveitis but definitive proof is lacking. Autoinflammatory disease, involving activated innate immune mechanisms, is considered causative in a second set of uveitis conditions. A place for infection in uveitis generally is proposed within a unifying concept for the pathogenesis of uveitis. Conclusion: Infection may be implicated directly or indirectly in many forms of noninfectious or undifferentiated uveitis. In addition to the growing recognition that foreign antigen, including reactivatable infectious agents, might hide within ocular tissues, the possibility that a dysregulated microbiome might generate T cells that cause immune-mediated ocular inflammation has now been demonstrated experimentally. An uncontrolled, overexuberant host immune response may cause continuing irreversible tissue damage even after the infection has been cleared.

Original languageEnglish
Pages (from-to)77-85
Number of pages9
JournalAmerican Journal of Ophthalmology
Volume189
DOIs
Publication statusPublished - 1 May 2018

Fingerprint

Uveitis
Autoimmunity
Infection
Posterior Uveitis
Blood-Retinal Barrier
Microbiota
Adaptive Immunity
Allergy and Immunology
Innate Immunity
Inflammation
T-Lymphocytes
Antigens

Cite this

Forrester, John V. ; Kuffova, Lucia ; Dick, Andrew D. / Autoimmunity, Autoinflammation, and Infection in Uveitis. In: American Journal of Ophthalmology. 2018 ; Vol. 189. pp. 77-85.
@article{418009a4e370432a895a84759bc2b4de,
title = "Autoimmunity, Autoinflammation, and Infection in Uveitis",
abstract = "Purpose: To review the pathogenesis of uveitis in light of recent advances in our understanding of innate and adaptive immune responses and their regulation. Design: Perspective. Methods: Methods included a review of prevailing views on the pathogenesis of uveitis and an analysis of developments in immunology that impact on its conceptual basis, particularly the concept of immunologic tolerance and its loss in autoimmunity. Importantly, the role of infection in the pathogenesis of uveitis is evaluated. Results: The results comprise a reappraisal of the pathogenesis of anterior vs posterior uveitis in the context of the blood-retinal barrier and its relation to autoimmune, autoinflammatory, and infectious uveitis. Autoimmunity is seen as a possible cause of certain forms of uveitis but definitive proof is lacking. Autoinflammatory disease, involving activated innate immune mechanisms, is considered causative in a second set of uveitis conditions. A place for infection in uveitis generally is proposed within a unifying concept for the pathogenesis of uveitis. Conclusion: Infection may be implicated directly or indirectly in many forms of noninfectious or undifferentiated uveitis. In addition to the growing recognition that foreign antigen, including reactivatable infectious agents, might hide within ocular tissues, the possibility that a dysregulated microbiome might generate T cells that cause immune-mediated ocular inflammation has now been demonstrated experimentally. An uncontrolled, overexuberant host immune response may cause continuing irreversible tissue damage even after the infection has been cleared.",
author = "Forrester, {John V.} and Lucia Kuffova and Dick, {Andrew D.}",
year = "2018",
month = "5",
day = "1",
doi = "10.1016/j.ajo.2018.02.019",
language = "English",
volume = "189",
pages = "77--85",
journal = "American Journal of Ophthalmology",
issn = "0002-9394",
publisher = "Elsevier",

}

Autoimmunity, Autoinflammation, and Infection in Uveitis. / Forrester, John V.; Kuffova, Lucia; Dick, Andrew D.

In: American Journal of Ophthalmology, Vol. 189, 01.05.2018, p. 77-85.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Autoimmunity, Autoinflammation, and Infection in Uveitis

AU - Forrester, John V.

AU - Kuffova, Lucia

AU - Dick, Andrew D.

PY - 2018/5/1

Y1 - 2018/5/1

N2 - Purpose: To review the pathogenesis of uveitis in light of recent advances in our understanding of innate and adaptive immune responses and their regulation. Design: Perspective. Methods: Methods included a review of prevailing views on the pathogenesis of uveitis and an analysis of developments in immunology that impact on its conceptual basis, particularly the concept of immunologic tolerance and its loss in autoimmunity. Importantly, the role of infection in the pathogenesis of uveitis is evaluated. Results: The results comprise a reappraisal of the pathogenesis of anterior vs posterior uveitis in the context of the blood-retinal barrier and its relation to autoimmune, autoinflammatory, and infectious uveitis. Autoimmunity is seen as a possible cause of certain forms of uveitis but definitive proof is lacking. Autoinflammatory disease, involving activated innate immune mechanisms, is considered causative in a second set of uveitis conditions. A place for infection in uveitis generally is proposed within a unifying concept for the pathogenesis of uveitis. Conclusion: Infection may be implicated directly or indirectly in many forms of noninfectious or undifferentiated uveitis. In addition to the growing recognition that foreign antigen, including reactivatable infectious agents, might hide within ocular tissues, the possibility that a dysregulated microbiome might generate T cells that cause immune-mediated ocular inflammation has now been demonstrated experimentally. An uncontrolled, overexuberant host immune response may cause continuing irreversible tissue damage even after the infection has been cleared.

AB - Purpose: To review the pathogenesis of uveitis in light of recent advances in our understanding of innate and adaptive immune responses and their regulation. Design: Perspective. Methods: Methods included a review of prevailing views on the pathogenesis of uveitis and an analysis of developments in immunology that impact on its conceptual basis, particularly the concept of immunologic tolerance and its loss in autoimmunity. Importantly, the role of infection in the pathogenesis of uveitis is evaluated. Results: The results comprise a reappraisal of the pathogenesis of anterior vs posterior uveitis in the context of the blood-retinal barrier and its relation to autoimmune, autoinflammatory, and infectious uveitis. Autoimmunity is seen as a possible cause of certain forms of uveitis but definitive proof is lacking. Autoinflammatory disease, involving activated innate immune mechanisms, is considered causative in a second set of uveitis conditions. A place for infection in uveitis generally is proposed within a unifying concept for the pathogenesis of uveitis. Conclusion: Infection may be implicated directly or indirectly in many forms of noninfectious or undifferentiated uveitis. In addition to the growing recognition that foreign antigen, including reactivatable infectious agents, might hide within ocular tissues, the possibility that a dysregulated microbiome might generate T cells that cause immune-mediated ocular inflammation has now been demonstrated experimentally. An uncontrolled, overexuberant host immune response may cause continuing irreversible tissue damage even after the infection has been cleared.

UR - http://www.scopus.com/inward/record.url?scp=85045886317&partnerID=8YFLogxK

U2 - 10.1016/j.ajo.2018.02.019

DO - 10.1016/j.ajo.2018.02.019

M3 - Article

VL - 189

SP - 77

EP - 85

JO - American Journal of Ophthalmology

JF - American Journal of Ophthalmology

SN - 0002-9394

ER -