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Year : 1979  |  Volume : 27  |  Issue : 3  |  Page : 9-11

Immune disorders of the eye

A. M. U. Institute of Ophthalmology J. N. Medical College, Aligarh (U.P.), India

Correspondence Address:
R Gogi
A.M.U. Institute of Ophthalmology, J.N. Medical College, Aligarh (U.P.)
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Source of Support: None, Conflict of Interest: None

PMID: 159867

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How to cite this article:
Gogi R. Immune disorders of the eye. Indian J Ophthalmol 1979;27:9-11

How to cite this URL:
Gogi R. Immune disorders of the eye. Indian J Ophthalmol [serial online] 1979 [cited 2020 Nov 27];27:9-11. Available from: https://www.ijo.in/text.asp?1979/27/3/9/31216

Immunology has always been involved in Ophthalmology. It was an essential part of the paper of Elsching[10] in his studies on antigenic action of the uveal pigment in cases of sympa­thetic ophthalmia. The antigenic nature of the human lens was discovered by Straub[29] and later confirmed by Verhoeff and Lemoine[30] Therefore, the credit for the present-day most fashionable term of autoimmunity also goes to these early ophthalmologists.

There are a number of peculiar anatomical, physiological and biochemical features of the eye which contribute a distinctive character which tends to modify and modulate the ocular immune response. Intraocular structures are devoid of lymphatic drainage and there is tight blood-aqueous barrier at the level of retinal capillaries, the pigment epithelium of retina, and the ciliary epithelium. The lens and the cornea are avascular structures. Therefore, intraocular structures suffer immunological isolation. This may prove beneficial or harmful to the ocular structures depending upon the products of immune response. Since there are no regional lymph nodes to drain intraocular structures, so the antigen sensitive lymphocytes migrate into the eye and in this way the uvea may act as an accessory lymph node. Lymph­ocytic infiltration of the uvea may therefore signify a physiological rather than a pathological response. Furthermore, rich autonomic nerve supply shows an abnormal vasomotor sensitivity. Therefore, a mild immunological insult to the eye, which may be ignored in other parts of the body, becomes a serious matter.

Basic Concept

Human lymphoid system has mainly two types of lymphocytes, that is, T-lymphocytes (Thymus dependent lymphocytes) and B-lympho­cytes (Bursa dependent lymphocytes). T-lymphocytes are responsible for cell mediated hypersensitivity or delayed hypersensitivity or cellular immunity. These cells liberate a chemi­cally active substance known as lymphokine. Where as B-lymphocytes are antibody forming cells and are responsible for humoral immunity. Both B and T-cells produce an immunological reaction on exposure to foreign protein. However, cccassionally these cells may become activated in response to one's own healthy tissue component. This is known as autoimmune disease.

Ocular lesions

Conventionally, hypersensitivity reactions are of four types, Type I, II, III, & IV. Recently another type known as stimulatory hypersensi­tivity has also been added and is involved in the production of thyrotoxic exophthalmos.

Type I Hypersensitivity

This is also known as immediate hypersensi­tivity or acute anaphylaxia. It is mediated by IgE immunoglobulin. The most commonly found conjunctival allergy i.e. Vernal Catarrh belongs to this group. Other examples include hay fever conjunctivitis, atopic conjunctivitis and drug allergy. The characteristic histologi­cal finding is marked eosinophil leucocyte infiltration.

Type II Hypersensitivity

Here in response to an antigen, antibodies are formed and the main antibody is IgG. Site of damage is determined by the antibodies. There is activation of complement which is responsible for the damage, that is why it is also known as Complement dependent hyper­sensitivity. Some of the typical lesions of this type of reaction include Mooren's ulcer, ocular pemphigus and pemphigoid, Corneal graft rejection and experimental immune retinitis.

Type III Hypersensitivity

Here antigen-antibody combine to make complexes. The distribution of tissue lesions is determined by the sites of formation of deposition of antigen-antibody complexes. Type III hypersensitivity is also known as immune­Complex disease. Endogenous uveitis is a common example. Other diseases of this group are erythema multiforme, corneal immune rings, phaco-allergic endophthalmitis, scleritis and episcleritis.

Type IV Hypersensitivity or cell-mediated allergy

A large number of diseases are believed to develop following a delayed hypersensitivity­reaction to a variety of exogenous and endogen­ous antigens. Sympathetic ophthalmia is often considered as the prototype. Other common diseases are, herpetic keratitis, optic neuritis, corneal graft rejection, certain bacterial, fungal, viral, protozal and parasitic infections. Con­trary to type I, II & III hypersensitivity reactions which are mediated by antibodies, the delayed hypersensitivity reactions are exclusively conduc­ted by T-lymphocyte population and are thus cell mediated. A cell mediated hypersensitivity is characterized by perivascular cuffing with lymphocytes, particularly in the early stage, and is followed by granulomatous inflammation. Variant of cell mediated hypersensitivity are recognized as "Retest reaction" and "Cutaneous Basophil Hypersensitivity" characterized by eosinophil and basophil leucocytic infiltration[32].

  References Top

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Rahi, A.H.S. & Tripathi, R.C., 1976, Proc. 1st Int. Symp. on Immunology and Immunopatho­logy of the eye, Strasbourg, 1974, Mod. Prob. Ophthal., Vol-16 Karger, Basels In Press.  Back to cited text no. 26
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Woods, A.C., 1961, Endogenous inflammations of the uveal tract, Williams & Wilkins, Baltimore.  Back to cited text no. 32


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