Abstract
Uveitis is a relatively confusing term since it implies
primary inflammation of the uveal tract. However, it
has become clear during the last few decades of
research into the causes of uveitis that the uveal tract
acts primarily as the conduit for the inflammatory
cells and the increased blood flow that accompany
inflammation targeted to other sites in the eye such
as the retina and sclera. Uveitis is, therefore, better
referred to as intraocular inflammation (l01).
A major problem in understanding the pathophysiology of 101 is that clinically there is a great variety
of presentations of apparently different conditions.
However, a significant unifying concept, at least from
the viewpoint of pathogenetic mechanisms, is that
many of the clinical manifestations of 101 can be
mimicked with models of experimental autoimmune
uveoretinitis (EAU) which utilise a single antigen.1
This is not to say that autoimmune mechanisms
account for most causes of 101 since the opposite is
probably true; rather, that the intraocular tissues,
particularly the retina and choroid, can respond to
challenge by foreign or autoantigen in only a limited
set of ways and that it should not be surprising that
there is considerable overlap in the clinical manifestations of many of these conditions. These concepts
have been discussed previously?.3
This paper aims to address a separate but related
problem: if the eye and its component tissues can
respond in only a limited set of clinical manifestations, why is there preferential localisation of
inflammation and tissue damage to discrete sites in
certain conditions?
primary inflammation of the uveal tract. However, it
has become clear during the last few decades of
research into the causes of uveitis that the uveal tract
acts primarily as the conduit for the inflammatory
cells and the increased blood flow that accompany
inflammation targeted to other sites in the eye such
as the retina and sclera. Uveitis is, therefore, better
referred to as intraocular inflammation (l01).
A major problem in understanding the pathophysiology of 101 is that clinically there is a great variety
of presentations of apparently different conditions.
However, a significant unifying concept, at least from
the viewpoint of pathogenetic mechanisms, is that
many of the clinical manifestations of 101 can be
mimicked with models of experimental autoimmune
uveoretinitis (EAU) which utilise a single antigen.1
This is not to say that autoimmune mechanisms
account for most causes of 101 since the opposite is
probably true; rather, that the intraocular tissues,
particularly the retina and choroid, can respond to
challenge by foreign or autoantigen in only a limited
set of ways and that it should not be surprising that
there is considerable overlap in the clinical manifestations of many of these conditions. These concepts
have been discussed previously?.3
This paper aims to address a separate but related
problem: if the eye and its component tissues can
respond in only a limited set of clinical manifestations, why is there preferential localisation of
inflammation and tissue damage to discrete sites in
certain conditions?
Original language | English |
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Pages (from-to) | 162-166 |
Number of pages | 5 |
Journal | Eye |
Volume | 11 |
Issue number | 2 |
DOIs | |
Publication status | Published - 1 Jan 1997 |