NIH-funded research R01 grant

STAT4-driven immune problems and poor wound healing in disabling pansclerotic morphea

Official title: Crosstalk of Immune Dysregulation and Impaired Wound Healing in inherited STAT4-mediated Autoinflammatory Disease

Funded at University of California, San Diego · NIH-11267975 · Data updated 2026-11-12

The team will try blocking overactive STAT4/JAK signaling to reduce inflammation and help wound healing for children with disabling pansclerotic morphea.

Quick facts

Grant typeR01 grant
Study typeNIH-funded research
Funding institutionUniversity of California, San Diego
NIH-funded
Lab location1 site (La Jolla, United States)
Project startFebruary 1, 2025
Project endJanuary 31, 2030
Funding year2026
Award (this year)$398,959
NIH project number5R01AI189984-02
Project IDNIH-11267975 on NIH RePORTER

Who could benefit from this research

Could help

Ideal candidates are children and other patients diagnosed with disabling pansclerotic morphea, especially those known to carry STAT4 gain-of-function variants.

Less likely to help

Patients with other forms of morphea that do not involve STAT4 or JAK-STAT signaling may not receive direct benefit from these findings.

What this research studies

This project focuses on disabling pansclerotic morphea (DPM), a rare childhood disease where a STAT4 gene change causes severe inflammation and poor skin and joint healing. Researchers will use patient samples, cell-based experiments, and animal models to study how the STAT4 gain-of-function mutation keeps immune signals like phosphorylated STAT4 and IL-6 turned on and impairs immune cell development and tissue repair. They will test whether JAK inhibitors can lower IL-6, reduce autoinflammation, and restore normal wound healing in the lab and in vivo. The team aims to connect those laboratory findings back to patients to inform potential targeted treatments.

Why it matters

Potential benefit: If successful, this work could point to targeted therapies (such as JAK inhibitors) that reduce inflammation and improve wound healing and survival for people with STAT4-mediated DPM.

How similar studies have gone: JAK inhibitors have shown benefit in other autoinflammatory and dermatologic conditions and the preliminary lab and animal data here suggest improved wound healing, though clinical proof in DPM remains limited.

Where this research is happening

  • University of California, San Diego
    La Jolla, United States
    Active

Researchers

  • Principal investigator: Broderick, Lori — University of California, San Diego
  • Study coordinator: Broderick, Lori

Related research

Other NIH-funded projects on the same topics.

About this research

  1. This is an active NIH-funded research project — typically early-stage science, not a clinical trial accepting patient enrollment.
  2. Some NIH-funded labs run parallel clinical studies or seek volunteers for related work. To check, contact the principal investigator or institution listed above.
  3. For full project details, budget, and progress reports, visit the official NIH RePORTER page.
Last reviewed 2026-11-14 by the Find a Trial editorial team. Information on this page is for educational purposes and is not medical advice. Always consult qualified healthcare professionals about clinical trial participation.