Ellen Cealey

Division of Rheumatology, Clinical Autoimmunity Center of Excellence, University of Michigan Medical School, Ann Arbor, MI 48109.

1 publication 2019 – 2019

What does Ellen Cealey research?

Ellen Cealey studies the effects of a protein called CD13, particularly in the context of rheumatoid arthritis. Her research explores how this protein is present in inflamed joints and how it can promote both the growth of new blood vessels and attract immune cells, which are significant factors in the development and progression of inflammation in joints. By examining the mechanisms of CD13, Cealey aims to find potential new treatments for various inflammatory joint diseases.

Key findings

  • Cealey's research demonstrated that injecting CD13 into mouse knees caused significant joint swelling and inflammation.
  • The study found that CD13 promotes the growth of new blood vessels in inflamed joints, which is crucial for the progression of rheumatoid arthritis.
  • Blocking the action of CD13 could present a new therapeutic approach for treating rheumatoid arthritis and similar inflammatory conditions.

Frequently asked questions

Does Dr. Cealey study rheumatoid arthritis?
Yes, Dr. Cealey's research focuses specifically on how the protein CD13 contributes to rheumatoid arthritis and other inflammatory joint diseases.
What treatments has Dr. Cealey researched?
Dr. Cealey is investigating the potential of blocking CD13 as a new treatment strategy for rheumatoid arthritis and related conditions.
Why is CD13 important in joint diseases?
CD13 is important because it helps promote inflammation and the growth of blood vessels in the joints, which are key processes in diseases like rheumatoid arthritis.

Publications in plain English

Angiogenic and Arthritogenic Properties of the Soluble Form of CD13.

2019

Journal of immunology (Baltimore, Md. : 1950)

Du Y, Lu C, Morgan RL, Stinson WA, Campbell PL +10 more

Plain English
Researchers found that a protein called CD13, which is released into fluid in inflamed joints, promotes the growth of new blood vessels and attracts immune cells to the joint—both hallmarks of rheumatoid arthritis. The protein works through its structure rather than its enzymatic function, and when injected into mouse knees, it triggered joint swelling and inflammation. This discovery suggests that blocking CD13 could be a new way to treat rheumatoid arthritis and other inflammatory joint diseases.

PubMed

Publication data sourced from PubMed . Plain-English summaries generated by AI. Not medical advice.