Corrections appended.
There are few things that can put a damper on an end of summer evening in upstate New York, but allergies are one of them. The classic watery eyes, incessant sneezing, and insatiable back of throat itch one feels while relaxing on Libe Slope or hiking to Second Dam can be attributed to little molecules called allergens, and our bodies response to them. Yet pollen isn’t the only thing that can send one running for a tissue or bathroom. Many compounds in the environment including plants, food and insect product can cause full scale immunological responses and Melissa Page ’20 has set out to better understand why.
Researching alongside Simon Freuh Ph.D. in the Elia Tait Wojno Lab of Immunology, Page has focused on exploring in detail the mechanisms behind the severe immune response caused by atopic dermatitis—a chronic inflammatory, skin disease that is a common skin-related allergy in dogs.
While this may seem like a very specific malady, the mechanisms that cause this response may be similar across all species, involving cells that can receive pro-allergic signals via a series of receptors after exposure to allergens. Through the study of a prostaglandin receptor called CRTH2, a lipid receptor found on a number of different pro-allergic immune cell types, Page hopes to investigate the vexing issues of allergic reactions in dogs, humans, and other species.
Page explained that her motivation for conducting allergy-related research came from her experience working with allergy development in children previously.
“After doing nutrition research, one summer, at University of Rochester, where I looked at microbiomes and allergy development in kids, I wanted to expand my work in the field of immunology,” she said.
Page started last year in the Tait Wojno lab and is now in the process of working on a research thesis on the role of prostaglandin receptors in allergic reactions.
CRTH2 is found on the membrane of CD4+ helper T-cells and other pro-allergic immune cells that initiate and perpetuate the body’s inflammatory response. When activated by allergens, CRTH2 instructs immune cells to migrate to inflamed tissue and to produce pro-inflammatory factors called cytokines such as interleukin 4 and interleukin 5.
Page has investigated this process in mice, using a mouse model of atopic dermatitis and mice with and without the gene that codes for the CRTH2 receptor. Page has compared the presence of cytokines and other immune cells through specific cell screening techniques in mice that have or lack CRTH2 in order to determine what the effects of CRTH2 deletion are.
Page is still in the process of analyzing her data, but it is possible that her findings will have similar implications and contribute some explanation to the mechanisms that cause atopic dermatitis in dogs and humans. These studies build on a previous discovery made by the Tait Wojno lab earlier this year. Through a study of atopic dermatitis in dogs, Page’s fellow researchers found that certain immune cells in the blood are increased in number in companion pet dogs with atopic dermatitis compared to non-allergic dogs. The patients came from the Cornell University College of Veterinary Medicine Hospital for Animals. How CRTH2 might control these immune cells remains to be determined, and Page’s research could shed light on this issue.
“My project may not give direct answers or save lives but a big part of immunology research is just gaining knowledge that helps to add to other aspects of the field,” Page said.
Through her research thesis, Page hopes to better understand the specific behavior of CRTH2 to unpack the intricacies of general allergen responses. Ultimately, this knowledge could inform clinical applications in a veterinary setting or even regarding human health.
Research specifics that involve important issues related to canine genetics, reproductive technologies, and animal research in general were corrected.