Ilene K. Gipson

Dr. Gipson studies the ocular surface. This structure, at the front of the eye, enables and protects vision. Therefore, diseases that affect it can be devastating, and are among the leading causes of blindness and vision impairment worldwide.

Dr. Ilene Gipson received her PhD from the University of Arkansas in l973. She began her career in vision research at the University of Oregon Health Sciences Center, where she became an Assistant Professor of Ophthalmology. In 1979, she was recruited to the Schepens Eye Research Institute (then the Eye Research Institute of the Retina Foundation). She rose through the ranks from Assistant to Senior Scientist at the Institute, and in 1997 became Professor of Ophthalmology at Harvard Medical School and also the Ocular Surface Scholar at the Institute. She is the recipient of numerous awards, including the MERIT Award from the National Eye Institute and the Research to Prevent Blindness Senior Scientific Investigator Award. In May, 2007, Dr. Gipson received The Friedenwald Award; this award is one of the two achievement awards given annually at the Association for Research in Vision and Ophthalmology meeting to honor the outstanding research of senior scientists in the basic or clinical sciences as applied to ophthalmology.

What is the ocular surface?

The ocular surface is the layer of cells at the front of the eye – those cells that come in contact with the outside world. These cells cover the cornea (the clear covering of the eye) and the conjunctiva (the white of the eye and the inner eyelids), and also form the lacrimal and Meibomian glands. Each layer of cells that form these surfaces is called an epithelium; they are shown in rose in the diagram. Each region of the ocular surface epithelium produces components that help form the tear film, which keeps the surface of the eye moist and protected from pathogen invasion.

How does the ocular surface enable vision?

The major way in which the ocular surface enables vision is that it bends (refracts) light so that the light can focus on the retina. The cornea is where most of the eye’s refraction occurs; the lens (through which the light travels after it goes throught the cornea) is not as powerful a light-bending structure. To bend light as much as the ocular surface on the cornea does, this surface must be both curved and exceptionally smooth. Maintaining this smooth, wet surface on the cornea requires the secretion the tear film. This film has an outer lipid layer, secreted by the Meibomian glands, that prevents the tears from drying out. The film also contains watery tears, produced by the lacrimal glands. Importantly, maintaining the smooth surface also requires keeping the tears and lipids in place on the epithelial surface.
The surface of the epithelia of the cornea and conjunctiva produces at its tear-film surface a class of molecules that help hold the watery layer onto the surface of the eye. These molecules are very hydrophilic or “water loving”. They act as sponges, keeping the tears on the ocular surface. They also provide a barrier that prevents entry of pathogens into the epithelium. This class of molecules is called mucins. Mucins are made by all of the wet epithelia of the body, notably the epithelia that are on the surface of the gastrointestinal, respiratory, and reproductive tracts (but not the skin). All of us who have had a bad cold know about the mucus that results from the infection. The major component of mucus is mucins. 
The Gipson laboratory is expert in mucin biology, primarily as these molecules relate to the ocular surface; however, the lab has also made major contributions regarding mucins and reproductive-tract function.

What diseases affect the ocular surface and interfere with its function of enabling vision?

A long list of diseases that affect the ocular surface can be compiled. Some of the major ones include dry eye diseases, infections, immune diseases that affect the ocular surface, and dietary deficiency of vitamin A (a problem in some developing countries).

How are mucins involved in these diseases?

The Gipson lab has demonstrated an alteration in epithelial surface mucins in several types of dry eye, and has data showing that loss of surface mucins allows penetrance into the corneal epithelium of the dyes that are used to diagnose dry eye disease. This indicates that mucins are lost from the epithelial surface in dry eye.
Recent data from the Gipson lab shows that these surface mucins provide a barrier, to prevent bacteria from sticking to the ocular surface cells. Because infections of the surface of the eye often occur if the surface of the eye is dry or injured, this implies that the mucin barrier has been removed or altered. In some of the immune-system diseases that affect the ocular surface, drying occurs with loss of mucins and, in animal models of vitamin A deficiency, mucin genes are less active, causing the loss of mucins on the ocular surface.

What have we learned from our studies that may be of use in preventing or treating these diseases?

We developed human ocular-surface epithelial cell-culture systems so that we can find factors that upregulate mucin gene expression, thereby enhancing protection and tear retention. We have found several agents that affect mucin production and removal from the ocular surface. We hope that, by understanding these processes, we will find new therapies for dry eye and for protecting those eyes that are at risk of infection.