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Hung Nguyen, PhD

Hung Nguyen, PhD

Brigham and Women’s Hospital

Research Project:
How T Lymphocyte Promotes Fibrosis in Fibrotic Interstitial Lung Disease

Grant Awarded:

  • Catalyst Award

Research Topics:

  • basic biologic mechanisms
  • immunology immunotherapy

Research Diseases:

  • interstitial lung disease
  • pulmonary fibrosis

Fibrosis, or scarring, affects many different diseases and is a major health problem. Fibroblasts are a main type of cell that causes fibrosis. Besides fibroblasts, immune cells also play an important part in fibrosis. We are studying how a specific immune cell called T lymphocyte promotes fibrosis in a lung disease called fibrotic interstitial lung disease, or fILD. We have found that patients with certain kinds of fILD have increased numbers of T cells and that these T cells are recruited to the lung by chemical signals called chemokines produced by fibroblasts. We found that a particular chemokine called CXCL12 is increased in fibroblasts from fILD patients and that it helps in attracting T cells to diseased lungs. We also found another protein called TWEAK that regulates the production of CXCL12. Our objective is to find out how TWEAK increases CXCL12 production so we can develop new treatments that decrease the number of T cells in fILD.

Catalyst Award, applied under the Dalsemer Award

 

Update: Fibrosis, or scarring, is a serious health problem that can affect many organs, including the lungs. In people with fibrotic interstitial lung disease (fILD), scar tissue builds up in the lungs, making it harder to breathe. Cells called fibroblasts are a major cause of this scarring, but immune cells also play an important role. Our research is studying how a type of immune cell called a T cell contributes to lung scarring. We found that people with certain forms of fILD have higher numbers of T cells in their lungs. These cells are drawn into the lungs by chemical signals released by fibroblasts. One of these signals, called CXCL12, is produced at higher levels in people with fILD and helps attract T cells to damaged lung tissue. We also discovered that another protein, called TWEAK, controls the production of CXCL12. Our goal is to understand how TWEAK works so that we can develop new treatments that reduce the number of harmful T cells in the lungs and slow or prevent further scarring.

Page last updated: September 21, 2026

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