|Year : 1979 | Volume
| Issue : 3 | Page : 9-11
Immune disorders of the eye
A. M. U. Institute of Ophthalmology J. N. Medical College, Aligarh (U.P.), India
A.M.U. Institute of Ophthalmology, J.N. Medical College, Aligarh (U.P.)
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Gogi R. Immune disorders of the eye. Indian J Ophthalmol 1979;27:9-11
Immunology has always been involved in Ophthalmology. It was an essential part of the paper of Elsching 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 and later confirmed by Verhoeff and Lemoine 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.
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.
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.
| References|| |
Allansmith, M.R. and O'Connor, G.R., 1969, Survey Ophth., 14, 367.
Bacsich P. & Wyburn, G.M., 1957, J. Anat. (Load), 91, 339.
Barker, C.F. & Billingham, R.E., 1973, Ciba foundation symposium 15, 79, Excerpta Medica, Amsterdam.
Block-Michel E., 1973-a, In uveitus: Immunologic and Allergic Phenomenon, Campinchi R., Faure J.P., Bloch-Michel E. & Haut J., p. 315.
Bloch-Michel E., 1973 b, In Uveitis: Immunologic and Allergic Phenomenon Campinchi R., Faure J.P., Bloch-Michel E. & Haut J., p. 155.
Char, D.H., Bergsma, D., Rabson, A.S., Albert, D.M. & Herberman, R.B., 1974, Invest Ophthal., 13, 198.
Char, D.H. & Herberman, R.B., 1974, Amer, Jour. Ophthal., 78, 40.
Coons, A.H. & Kaplan, M.H., 1950, Jour. Exp. Med., 91, 1.
Dumonde, D.C., 1970, Proc. Roy. Soc. Med., 63, 899.
Elsching, A., 1910, Graefes Arch. Ophthal., 75, 459.
Fessel, W.J., 1962, Amer. Jour. Ophthal., 53, 640.
Chose, T., Quigler, J.H., Landrigan, P.L. and Asif, A., 1973, Brit. Jour. Ophthal., 57, 897.
Gogi, R., Rahi, A H.S., & Garner, A., 1979, Histopathology, 3, 51.
Hellstorm, I , Sjogren, H.O., Warner, G. & Hellstorm, K.E., 1971; Inst. Jour. Cancer., 7, 226.
15. Hutchin, P., 1968, Surg. Gynec. Obstet., 126, 1331.
Khodadoust, A.A., & Silverstein, A.M., 1969, b, Invest. Ophthal., 8, 180,
Little, J., Ikeda, A., Zwaqn, J & Langman, J., l965, Exp. Eye Res., 4. 187.
Marak, G.E.. Aye, MS. & Alepa, F.P., 1973, Invest. Ot hthal., 12, 380.
Maumenee, A.E., 1973, Ciba foundation Symposium, 15, p. 5, Excerpta Medica, Amsterdam.
Meclellan B.H., Witney, C.R., Newman, L.P. & Allansmith, M.R., 1973, Amer. Jour. Ophthal., 76, 89.
Parks, J.J., Leibowitz, H.M.I. & Maumenee, E.A., 1962, Jour. Imnmnol, 89, 323.
Rahi, A.H.S. 1970, Brit. Jour. Ophthal., 54, 441.
Rahi, A.H.S. 1973, Brit. Jour. Ophthal., 57, 904.
Rahi, A.H.S. & Chignell, A.H, 1975, Trans. Ophthal. Soc. U.K., 95, 180.
Rahi, A.H.S. and Garner, A., 1976, Immunopathology of the eye, Blackwell Scientific Publications, Oxford.
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.
Russel, A.S., 1976, Jour. Insect. Diseases, 129, 142.
Sector, W.G. & Heesom N., 1969, Jour. Path., 98, 31.
Straub, M., 1919, de Bussy, Amsterdam.
Verhoeff, F.H. Lemoine, A.N., 1922, Acta. Int. Congress Ophthal., Washington, p. 245.
Wong, V.G., Anderson, R. & O'Brien, P.J., 1971, Amer. Jour Ophthal., 72, 960.
Woods, A.C., 1961, Endogenous inflammations of the uveal tract, Williams & Wilkins, Baltimore.