It is most commonly associated with HLA-B27, which has important features: HLA-B27 AAU can be associated with ocular inflammation alone or in association with systemic disease. HLA-B27 AAU has characteristic clinical features including male preponderance, unilateral alternating acute onset, a non-granulomatous appearance, and frequent recurrences, whereas HLA-B27 negative AAU has an equivalent male to female onset, bilateral chronic course, and more frequent granulomatous appearance. Rheumatoid arthritis is not uncommon in Asian countries as a significant association of uveitis. Noninfectious or autoimmune causes
Sympathetic ophthalmia
Behçet disease
Crohns disease
Fuchs heterochromic iridocyclitis
Granulomatosis with polyangiitis
HLA-B27 related uveitis
Spondyloarthritis (especially seen in ankylosing spondylitis)
Juvenile idiopathic arthritis
Sarcoidosis
Tubulointerstitial nephritis and uveitis syndrome

Infectious causes
Uveitis may be an immune response to fight an infection inside the eye. While representing the minority of patients with uveitis, such possible infections include:

brucellosis
herpesviruses (herpes zoster ophthalmicus - shingles of the eye)
leptospirosis
Lyme disease
presumed ocular histoplasmosis syndrome
syphilis
toxocariasis
toxoplasmic chorioretinitis
tuberculosis
Zika fever

Associated with systemic diseases
Systemic disorders that can be associated with uveitis include:
Enthesitis
Ankylosing spondylitis
Juvenile rheumatoid arthritis
psoriatic arthritis
reactive arthritis
Behçets disease
inflammatory bowel disease
Whipples disease
systemic lupus erythematosus
polyarteritis nodosa
Kawasakis disease
chronic granulomatous disease
sarcoidosis
multiple sclerosis
Vogt–Koyanagi–Harada disease

Drug related side effects
Rifabutin, a derivative of Rifampin, has been shown to cause uveitis. Several reports suggest the use of quinolones, especially Moxifloxacin, may lead to uveitis. White Dot syndromes
Occasionally, uveitis is not associated with a systemic condition: the inflammation is confined to the eye and has unknown cause.
In some of these cases, the presentation in the eye is characteristic of a described syndrome, which are called white dot syndromes, and include the following diagnoses:

acute posterior multifocal placoid pigment epitheliopathy
birdshot chorioretinopathy
multifocal choroiditis and panuveitis
multiple evanescent white dot syndrome
punctate inner choroiditis
serpiginous choroiditis
acute zonal occult outer retinopathy

Masquerade syndromes
Masquerade syndromes are those conditions that include the presence of intraocular cells but are not due to immune-mediated uveitis entities. These may be divided into neoplastic and non-neoplastic conditions. Non-neoplastic:retinitis pigmentosa
intraocular foreign body
juvenile xanthogranuloma
retinal detachmentNeoplastic:retinoblastoma
lymphoma
malignant melanoma
leukemia
reticulum cell sarcoma

Pathophysiology
Immunologic factors
Onset of uveitis can broadly be described as a failure of the ocular immune system and the disease results from inflammation and tissue destruction. Uveitis is driven by the Th17 T cell sub-population that bear T-cell receptors specific for proteins found in the eye. These are often not deleted centrally whether due to ocular antigen not being presented in the thymus (therefore not negatively selected) or a state of anergy is induced to prevent self targeting.Autoreactive T cells must normally be held in check by the suppressive environment produced by microglia and dendritic cells in the eye. These cells produce large amounts of TGF beta and other suppressive cytokines, including IL-10, to prevent damage to the eye by reducing inflammation and causing T cells to differentiate to inducible T reg cells. Innate immune stimulation by bacteria and cellular stress is normally suppressed by myeloid suppression while inducible Treg cells prevent activation and clonal expansion of the autoreactive Th1 and Th17 cells that possess potential to cause damage to the eye.