NPF-Funded Research

Th9-Endothelial Crosstalk Promotes Cardiovascular Disease in Patients with Psoriasis

A headshot of Daniella Schwartz, M.D.

Principal Investigator: Daniella Schwartz, M.D.
University of Pittsburgh

Grant Mechanism: Translational Research Grant
Funding Amount: $200,000
Project Start Date: August 1, 2021
Project End Date: July 30, 2023
Status: Active
Keywords: Basic Science, Cardiovascular Disease, Immunology, Psoriasis

Project Summary:

Inflammatory cytokines are molecules that cells secrete to mount an immune response. When immune cells inappropriately produce cytokines, patients can develop autoimmune or inflammatory diseases. In psoriasis, inflammatory cytokines like interleukin-17A (IL-17A) and IL-23 promote inflammation in the skin, joints, and heart. Current cytokine-blocking therapies are very effective for psoriatic rash but do not work as well for symptoms outside the skin – including arthritis and cardiovascular disease. This leads us to believe that other cytokines contribute to psoriatic inflammation outside the skin. We found that T helper 9 (Th9) cells, which produce the inflammatory cytokine IL-9, are elevated in patients with psoriasis. Patients with psoriasis and heart disease have more Th9 cells than patients without heart disease, and Th9 cells are found inside diseased blood vessels in the heart. IL-9 causes dysfunction in the cells that line the blood vessel walls. We would like to study these findings in patients with psoriatic heart disease, and in mouse models of psoriatic heart disease. Ultimately, we would like to block IL-9 in order to prevent heart disease in patients with psoriasis.

Researcher Profile:

The Schwartz lab studies a cytokine called IL-9, which links allergic and rheumatic diseases through regulation of lymphocytes, eosinophils, and mucosal barrier function. Research in the Schwartz lab is focused on defining the regulation and biological functions of IL-9 in the context of autoimmune and autoinflammatory conditions. We also try to expand the spectrum of rheumatic diseases by studying rare inborn errors of immunity that link allergic, autoimmune, and autoinflammatory pathologies. This includes the monogenic disease haploinsufficiency of A20 (HA20), an inborn error of ubiquitination that can cause severe autoinflammation, autoimmunity, immunodeficiency, and clinical allergy.

Impact of NPF-Funded Research

The NPF has awarded over $30 million in research funding in recent years, with immeasurable impact on our community.

Read more

We Need Your Help

With your gift we can fund even more research to get better treatment and diagnostic options and someday, a cure.

Help fund critical research

NPF-Funded Research

Discover our other active research projects.

Learn more

Stay in the Know

Expert tips, can’t-miss events, and the latest news, straight to your inbox.

National Health Council Standards of ExcellenceCharity NavigatorCommunity Health Charities logo

Copyright © 1996-2023 National Psoriasis Foundation/USA

Duplication, rebroadcast, republication, or other use of content appearing on this website is prohibited without written permission of the National Psoriasis Foundation (NPF).

NPF does not endorse or accept any responsibility for the content of external websites.

NPF does not endorse any specific treatments or medications for psoriasis and psoriatic arthritis.

We use cookies to offer you a better experience and analyze our site traffic. By continuing to use this website, you consent to the use of cookies in accordance with our Privacy Policy.