Shervin Assassi
University of Texas Health Science Center at Houston, TX·Medicine & Clinical Research
Systemic sclerosis (SSc), also called scleroderma, is a serious disease in which the immune system attacks the body and tissues such as the skin become scarred and stiff, a process called fibrosis. There are few effective treatments, partly because it is unclear how the overactive immune system drives fibroblasts, the cells that produce scar tissue.
- Fields
Medicine & Clinical Research
Microbiology & Immunology
Genetics
- Topics
systemic sclerosis
SSc
scleroderma
- Grants
- 1 known grant, through Apr 2028
What they work on
- Determine how much removing Irf7 specifically from fibroblasts reduces skin fibrosis, in bleomycin-induced and Tsk1 mouse models of dermal fibrosis.
- Define how IRF7, an interferon-induced transcription factor, changes SMAD3-driven gene activity after TGFβ stimulation, using human fibroblast lines with IRF7 overexpression or deletion and ChIP- and RNA-sequencing.
- Relate the interferon signature in SSc patients' blood to IRF7 levels in their skin tissue and dermal fibroblast subpopulations, using bulk and single-cell RNA sequencing.
More about the research
Understanding that link could reveal new targets for therapy.
Why it matters
People with systemic sclerosis face high rates of illness and death and have few effective treatment options. If IRF7 proves to be the link between immune overactivation and scarring, it could become a more targeted point for therapy. The work could also explain how the interferon signature measured in patients' blood relates to what happens in their skin.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Mengqi Huang
University of Pittsburgh, PA·Medicine & Clinical Research·Early-career
Identify the DNA control regions (cis-regulatory elements) that regulate the TGF-β3 gene in skin fibroblasts from patients with systemic sclerosis.
John Varga
University of Michigan, MI·Medicine & Clinical Research
Map where CD38, an immune-cell enzyme that breaks down the energy molecule NAD, is expressed in systemic sclerosis patient biopsies, and determine its cell type-specific role in fibrosis using engineered mice and disease models.
Ryan Driskell
Washington State University, WA·Biology
Test whether Lef1, a Wnt-pathway transcription factor, is the master regulator of newborn papillary fibroblast function by switching it on in adult mouse skin fibroblasts and using wounding and chamber grafting assays to see if scarring gives way to regeneration.
The school
University of Texas Health Science Center at Houston: 25 labs on PI Pages, $419M a year on research, 340 research doctorates a year.
More about University of Texas Health Science Center at Houston
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