Ananda W Goldrath
University of California-San Diego, CA·Microbiology & Immunology
After an infection clears, the immune system keeps a small set of memory T cells that can respond faster if the same germ returns. CD8 T cells, immune cells that directly kill infected or cancerous cells, form several kinds of memory.
- Fields
Microbiology & Immunology
Biology
Genetics
- Topics
CD8 T cells
memory T cells
Hic1
- Grants
- 2 known grants, through Oct 2028
What they work on
- Define how the transcriptional repressor Hic1 regulates the formation and maintenance of tissue-resident memory CD8 T cells, and identify the infection-induced signals that turn Hic1 on.
- Map Hic1's place in the network of gene regulators that keeps CD8 T cells resident in the small intestine after acute viral infection.
- Determine how tissue-specific programming shapes the ability of resident memory T cells to multiply and contribute to secondary memory responses.
- Test the role of Srebp2, a transcription factor that switches on cholesterol-making genes, in effector and memory CD8 T cells, and identify which cholesterol pathway intermediates and products tissue-resident memory T cells need.
- Place Srebp2 within the regulatory network that drives small-intestine resident memory T cells, and determine how known tissue cues that induce these cells affect Srebp2 expression.
More about the research
Some keep circulating through the blood and lymph nodes. Others, called tissue-resident memory T cells (TRM), settle permanently in organs such as the small intestine. There they guard against reinfection at the sites where germs enter, though in some cases they can also contribute to tissue damage in chronic infection and autoimmunity. The lab's two projects ask how CD8 T cells adapt to life inside a particular tissue. One project examines the gene-control programs that make a T cell a resident. The other examines the metabolic changes that allow it to survive there.
Why it matters
Vaccines and immune therapies work best when protective T cells are present where infections and tumors arise. Identifying the gene regulators, such as Hic1, and the metabolic pathways, such as Srebp2-driven cholesterol synthesis, that keep memory T cells in tissues could reveal new targets for designing tissue-tailored protective and therapeutic vaccines against infections and cancers.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Nu Zhang
University of Texas Health Science Center at San Antonio, TX·Microbiology & Immunology
Determine how TRM-stem cells, Tcf-1+ stem-like CD8+ T cells that become resident in tumor-draining lymph nodes, are related to other T cell subsets there, by tracking tumor-specific T cells in mouse tumor models.
James B Mclachlan
Tulane University of Louisiana, LA·Microbiology & Immunology
Determine how intradermal immunization with the detoxified enterotoxin adjuvant dmLT combined with bacterial outer membrane vesicles directs vaccine-specific T cells to mucosal tissues, tracked with MHC class I and II tetramers.
Ryan Nelson
University of Minnesota, MN·Microbiology & Immunology·Early-career
Define how allergen-specific regulatory T cells that stay in the lung suppress Th2 resident memory T cells, characterizing their location, persistence, suppressive strength and gene expression in a house dust mite mouse model of asthma.
The school
University of California-San Diego: 84 labs on PI Pages, $1.9B a year on research, 637 research doctorates a year.
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