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JAMES H. ELLIOTT, MD; HOWARD M. LEIBOWITZ, MD

Arch Ophthalmol. 1965;73(4):519-527.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

It has been shown experimentally that the cornea is capable of supporting two types of hypersensitivity phenomena.¹ The first type appears to be mediated by immunologically competent mononuclear cells, the second type by circulating antibodies.

When a soluble protein antigen is used to sensitize the cornea, the cellular-mediated response is manifest grossly by a transient dilatation of the circumlimbal vessels and a diffuse ground-glass opacification of the cornea. In contrast, the antibody-mediated corneal hypersensitivity reaction presents as a grossly discernible, white ring of opacification. The ring is composed of antigen-antibody complexes and inflammatory cells and is accompanied by dilatation of perilimbal vessels and corneal neovascularization.

Like the experimentally produced types of corneal hypersensitivity, the rejection of homologous and heterologous corneal grafts is thought to be immunologic in nature.^2-5 However, though circulating antibodies are often implicated in the rejection response, a ring reaction has never been reported.

The present . . . [Full Text PDF of this Article]

Author Affiliations
Boston

From the Howe Laboratory of Ophthalmology, Harvard University Medical School, Massachusetts Eye and Ear Infirmary.

Footnotes
Submitted for publication Sept 18, 1964.

Reprint requests to 243 Charles St, Boston, Mass 02114 (Dr. Elliott).

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