A uvéite is a Inflammation of the Uvée (iris, body cilaires and/or Choroïde).
Types
There exist 3 principal types of uvéite:- former: appears primarily on the level of the former room;
- intermediate: primarily at the level of the glazed former one;
- posterior: at the level of the glazed posterior one and retina.
And to finish the panuvéite which corresponds to a uvéite total which is however rarer.
Causes
One meets the uvéite in the rhumatologic diseases primarily:- spondylite ankylosante
- the syndrome of Reiter
- psoriatic arthritis
- youthful arthritis rhumatoïde.
In many cases, the cause is not found.
Symptoms
- ocular pain
- whimperings
- photophobia
- scrambled vision
- red eye
External bonds
- www.uveitissociety.org
- medlineplus
- www.uveitis.org
uvéite is an ignition of the Uvée (iris, body cilaires and/or Choroïde).
Eye is site immunologiquement privileged, i.e. that the product of the immunizing response is refreiné within this body as well as possible to save the various fabrics which compose it, in the ultimate goal preserving the transparency or the neurosensory function which is associated for them. The factors making it possible to moderate the ocular answer immune are multiple. Initially, these mechanisms are related to the anatomical structure of the eye: The concept of barriers hémato-eyepieces is known of long time. Theoretically, those avoid not only the passage of the ocular antigens in systemic circulation but also limit the penetration of immunizing cells circulating inside the ocular sphere. N the other hand, there exists a relative antigenic sequestration: the immune system is “blind” with ocular proteins. Nevertheless, this blindness is not complete: at the time of the thymopoïèse, there exists a thymique expression of certain ocular antigens (Charukamnoetkanok P 1998). In addition, like other sites immunologiquement privileged (brain, placenta, testicle) the intraocular structures do not have a systematized lymphatic drainage and the ocular antigen delivery to the regional ganglia is some thus limited. This modifies the environment of the antigenic presentation and thus the quality of the answer immune. Nevertheless, the anatomical characteristics of the ocular sphere are insufficient to explain this control of the answer immune. One can easily design that it will be necessary to control an infection will intra ocular by an immunizing surge of cells, in particular the lymphocytes T. In fact, it is established that this barrier hémato-eyepiece is not insuperable, since the adoptive transfer of lymphocytes T of Lewis rats immunized against the antigen S (Ag-S) retinal causes a uvéite at the receiver. (Rozenszajn 1986). This permeability of the barriers is granted to the lymphocytes T activated (Pendergast 1998). But so in certain situations this surge of lymphocytes can prove to be essential, the eye will have to control the inflammatory reaction which they involve, in order to preserve its neurosensory function. The barriers hémato-eyepieces not being hermetic, other mechanisms endoculaires are able to decontaminate the potentially noxious elements of the answer immune for the visual function. It is first of all about microenvironnement the intraocular immunomodulator, associating soluble factors present in the aqueous humor (TGF-β, VIP, α-MSH, MIF, IT 1R antagonists) and the membrane expression of molecules immunomodulatrices on the cells bordering the former room of the eye. An increased apoptose of the lymphocytes which reach the zones of immunizing privilege was noted (Dai 2005). This mechanism would be mainly assured by the interaction CD95 (Dick 1999) with its ligand CD178, expressed in a way constitutive on the level of the corneal endothelium, iris, body ciliaire and retina (Griffith 1995). Moreover, CD95 and CD178 are both found increased in soluble forms during the uvéites (Sugita 2000). Lastly, to that a “deviation” of the answer immune with respect to antigens present is added in the former room (but also glazed and subretinal space), baptized ACAID (Anterior Chamber Associated Immune Deviation), which support a cellular answer CD8+ cytotoxic and an answer humorale producing antibodies not fixing the complement, limiting on the contrary the answer of delayed the over-sensitiveness type and the production of antibody fixing the complement. This phenomenon of deviation was evoked in the auto-immune experimental uvéite (WATER) induced by the systemic injection of Interphotorecepror Binding Protein (IRBP), noting that mice sensitive to the uvéite were preserved by it when the antigen was injected beforehand into the former room. The ACAID is organized according to a oculo-splenic axis. The dendritic cells and the ocular macrophages present at the level of the body ciliaire and the iris collect the antigen then migrate by the means of the trabéculum and the aqueous veins in systemic circulation before gaining spleen. The macrophages carrying this message of ACAID are associated to the F4/80 marker. At the splenic level, these cells presenters of antigen (CPAg) will present the antigen to the cells NKT, which will activate regulating cells CD8+ which are then able to gain the eye and to remove there the answer of delayed over-sensitiveness of Th1 type. Nature and conditioning ocular private individuals of CPAg play big role in the induction of the ACAID. Thus, the injection of systemic dendritic cells beforehand conditioned in vitro by aqueous humor or of TGF-β induces a skewed answer similar to the ACAID. Nevertheless, if the model of ACAID is relatively well defined in the mouse, it has until now never clearly authenticated at the man.
At the time of a uvéite, the mechanisms of the “immunological privilege” ocular are unfortunately put at fault. This inflammatory state can result from an intraocular infection, but can be related to noninfectious causes, in particular in answer to antigens of self. The anatomical barriers as well as the ACAID make it possible to establish a relative immunological ignorance of the ocular antigens on behalf of the organization. This ignorance can be raised in two circumstances: an initial rupture of the anatomical barriers involving an autoimmunization, as one can note it at the time of uvéites phako-antigenic, where the patient immunizes himself against his own proteins cristalliniennes, normally isolated from the remainder of the organization by the capsule of the crystalline lens. In the second case, the autoimmune uvéites result from the surge will intra ocular of activated clones lymphocytaires car-reagents, this is the model of the UAE (example more studied) in the mouse after immunization at by the retinal S-Antigen in particular. These animal models highlighted several anomalies of at the time of a uvéite. There exists a rupture of the barrier hémato-eyepiece: Ohta could show an increase in the ocular protein concentrations and cells during the UAE (Ohta 1999). This model of UAE shows a loss of the immunosuppressive properties of the aqueous humor, which does not manage any more to inhibit the proliferation of the peripheral lymphocytes, contrary to the pilot aqueous humor. This loss of inhibition would be médiée by the pro-inflammatory IL-6, cytokine, since its ocular concentration is increased. Its action would be exerted by the intermédaire of an inhibition of the action of TGF-β, whose rate is also increased. This effect of the IL-6 is reversible by the administration of an inhibiting antibody. Lastly, the IL-6 causes the loss of the ACAID, authorizing the ocular CPA then to activate lymphocytes in periphery, and thus to pack the ocular ignition. To the man, only some studies related to the analysis of the cytokines present in the ocular mediums during the uvéites. -->
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