Laurie Harrington
University of Alabama at Birmingham, AL·Microbiology & Immunology
Autoimmune and chronic inflammatory diseases are becoming more common in the United States and worldwide, and for most of them nobody knows what starts the disease. The leading idea is that genes and environment combine to make some people susceptible.
- Fields
Microbiology & Immunology
Medicine & Clinical Research
Genetics
- Topics
Th17 cells
CD4 T cells
autoimmunity
- Grants
- 1 known grant, through Jul 2030
What they work on
- Determine how the transcription factor STAT4 directs the accumulation of Th17 cells, a pro-inflammatory CD4 T cell subset, in inflamed peripheral tissues.
- Test whether the STAT4/IL-10 axis within Th17 cells governs whether inflammation becomes chronic, since IL-10 is the signal that anti-inflammatory Th17 cells use to restrain tissue damage.
- Define at the molecular level how STAT4 drives differentiation of pathogenic Th17 cells while suppressing the emergence of their anti-inflammatory counterparts.
- Evaluate the hypothesis that STAT4 is a master regulator of IL-23-dependent inflammatory and autoimmune disease, connecting the gene variants flagged by genome-wide association studies to Th17 cell behavior.
More about the research
Large genetic surveys comparing patients to healthy people — genome-wide association studies — have repeatedly flagged the same immune genes, among them the signaling molecule IL-23, the inflammatory T cells it supports, and a gene called STAT4, which encodes a transcription factor that relays signals from outside a cell to the genes it turns on. Exactly how STAT4 contributes to autoimmunity is unknown, and this project sets out to define its job in disease.
Why it matters
Multiple sclerosis, inflammatory bowel disease and related chronic inflammatory conditions are driven in part by CD4 T cells, and current therapies do not work for everyone. Pinpointing how STAT4 tips Th17 cells toward damaging rather than protective behavior could reveal a common control point shared across several autoimmune diseases, which may inform more targeted ways to dampen harmful inflammation while sparing protective immunity.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Sankar Ghosh
Columbia University, NY·Microbiology & Immunology
Determine the molecular mechanism by which the long non-coding RNA lnc15 post-transcriptionally sets the level of Tbet messenger RNA, a master regulator of T cell identity.
Mandy J Mcgeachy
Cornell University, NY·Microbiology & Immunology
Determine how the interaction between PIP5K1a, an enzyme making the nuclear lipid PIP2, and ARS2, an mRNA cap-binding protein, is regulated as Th17 cells differentiate, using primary human T cells and CD28-humanized CD28A210P mice.
Ting Fu
University of Wisconsin-Madison, WI·Microbiology & Immunology
Determine how host- and microbe-derived bile acids generated during inflammation and tumor growth shape gut macrophages and their crosstalk with T cells and intestinal stem cells.
The school
University of Alabama at Birmingham: 45 labs on PI Pages, $866M a year on research, 166 research doctorates a year.
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