Uveitis pathophysiology

Jump to navigation Jump to search

Uveitis Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Uveitis from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

X Ray

CT

MRI

Ultrasound

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Uveitis pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Uveitis pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Uveitis pathophysiology

CDC on Uveitis pathophysiology

Uveitis pathophysiology in the news

Blogs on Uveitis pathophysiology

Directions to Hospitals Treating Uveitis

Risk calculators and risk factors for Uveitis pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Tarek Nafee, M.D. [2]

Overview

The exact pathogenesis of uveitis is not fully understood. It is thought that uveitis is mediated by a genetic predisposition and an acquired cross immunity to infectious agents, or cross immunity to self-antigens due to underlying autoimmune diseases. From 35% up to 50% of cases of uveitis are idiopathic.[1][2]Development of uveitis is hypothesized to be the result of a genetic predisposition for acquiring the disease. Contributions of several Human Leukocyte Antigen (HLA) alleles are most commonly implicated.[2][3]

Pathogenesis

The exact pathogenesis of uveitis is not fully understood. It is thought that uveitis is mediated by a genetic predisposition combined with cross immunity to infectious agents, or cross immunity to self-antigens due to underlying autoimmune diseases. Up to 35% of cases of uveitis are idiopathic.[1][2] Uveitis, in the setting of underlying infectious diseases, is hypothesized to be secondary to a T-cell mediated hypersensitivity reaction resulting in immunoactivating cytokine production by proliferating Tн17 and Tн1 cells.[3][4] A similar mechanism is hypothesized for autoimmune etiologies of uveitis with the exception of an unknown source of the triggering antigen.[5][6][7][8]

Genetics

Development of uveitis is hypothesized to be the result of a genetic predisposition for acquiring the disease. Contributions of several Human Leukocyte Antigen (HLA) alleles are most commonly implicated. This includes, HLA-B27 in seronegative spondyloarthropathies, HLA-A29 in birdshot chorioretinopathy, HLA-B51 in Behcet syndrome and multiple sclerosis, HLA-B8, HLA-DR15, and HLA-DR2.[2][3]

Associated Conditions

The following conditions are associated with uveitis:[1][2][9]

Gross Pathology

The following are images of the gross pathology of uveitis:[10][11]

Microscopic Pathology

The following are images of the microscopic pathology of uveitis:[12]

References

  1. 1.0 1.1 1.2 Rodriguez A, Calonge M, Pedroza-Seres M, Akova YA, Messmer EM, D'Amico DJ; et al. (1996). "Referral patterns of uveitis in a tertiary eye care center". Arch Ophthalmol. 114 (5): 593–9. PMID 8619771.
  2. 2.0 2.1 2.2 2.3 2.4 Guly CM, Forrester JV (2010). "Investigation and management of uveitis". BMJ. 341: c4976. doi:10.1136/bmj.c4976. PMID 20943722.
  3. 3.0 3.1 3.2 Przeździecka-Dołyk J, Węgrzyn A, Turno-Kręcicka A, Misiuk-Hojło M (2016). "Immunopathogenic Background of Pars Planitis". Arch Immunol Ther Exp (Warsz). 64 (2): 127–37. doi:10.1007/s00005-015-0361-y. PMC 4805694. PMID 26438050.
  4. Urban B, Bakunowicz-Łazarczyk A, Michalczuk M (2014). "Immune recovery uveitis: pathogenesis, clinical symptoms, and treatment". Mediators Inflamm. 2014: 971417. doi:10.1155/2014/971417. PMC 4096001. PMID 25089078.
  5. Sun D, Liang D, Kaplan HJ, Shao H (2015). "The role of Th17-associated cytokines in the pathogenesis of experimental autoimmune uveitis (EAU)". Cytokine. 74 (1): 76–80. doi:10.1016/j.cyto.2014.12.017. PMC 4457592. PMID 25742774.
  6. Bi HS, Liu ZF, Cui Y (2015). "Pathogenesis of innate immunity and adaptive immunity in the mouse model of experimental autoimmune uveitis". J Chin Med Assoc. 78 (5): 276–82. doi:10.1016/j.jcma.2015.01.002. PMID 25769932.
  7. Horai R, Caspi RR (2011). "Cytokines in autoimmune uveitis". J Interferon Cytokine Res. 31 (10): 733–44. doi:10.1089/jir.2011.0042. PMC 3189550. PMID 21787221.
  8. Ke Y, Liu K, Huang GQ, Cui Y, Kaplan HJ, Shao H; et al. (2009). "Anti-inflammatory role of IL-17 in experimental autoimmune uveitis". J Immunol. 182 (5): 3183–90. doi:10.4049/jimmunol.0802487. PMC 3275433. PMID 19234216.
  9. American Academy of Ophthalmology EyeWiki(2015)http://eyewiki.aao.org/Category:Uveitis
  10. Wikipedia Uveitis(2006)https://en.wikipedia.org/wiki/Uveitis#/media/File:Hypopyon.jpg
  11. University of Michigan Eyes Have It(2009)http://kellogg.umich.edu/theeyeshaveit/red-eye/anterior-uveitis.html
  12. Arevalo JF, Garcia RA, Al-Dhibi HA, Sanchez JG, Suarez-Tata L (2012). "Update on sympathetic ophthalmia". Middle East Afr J Ophthalmol. 19 (1): 13–21. doi:10.4103/0974-9233.92111. PMC 3277011. PMID 22346110.

Template:WH Template:WS