Gianna Hammer
Associate Professor of Microbiology & Immunology
Gut, Gut-brain, Inflammation, Colorectal Cancer, Innate Immunity, Enteric Pathogens, Innate-like T Cells
Molecular Biology Program
Education
B.S. Eastern Washington University
Ph.D. University of California, Berkeley
Research
We are a “gut lab”—if it lives, visits, or issomehowinfluenced by the gut, then we want to understand it. I viewthe gut as a resource from which to glean information about host-microbe dynamics, the balance that enablespeacewith microbes, and how the balance must be swayed to battle againstmicrobialpathogens and cancer. Wehave ongoing research investigating the gut-brain axis, the gut-liver axis, the healthy gut, the inflamed gut, thepathogen-infected gut, and colorectal cancer. If there is any unifying principle that we have learned from thesestudies it would be that the gut has its own rules for host-microbe interactions, and this set of rules is unique foreach setting. As mucosal immunologists, we thrive in this arena.
References (Selected Publications)
- Huang HI, Xue Y, Jewell ML, Tan CY, Theriot B, Aggarwal N, Dockterman J, Lin YD, Schroeder EA, Wang D, Xiong N, Coers J, Shinohara ML, Surana NK, Hammer GE. A binary module for microbiota-mediated regulation of gd17 cells, hallmarked by microbiota-driven expression of programmed cell death protein 1 (2023). Cell Reports Aug;42(8):112951. doi: 10.1016/j.celrep.2023.112951. PMCID: PMC10588736
- Huang H, Jewell ML, Youssef N, Huang M, Hauser ER, Fee, BE, Rudemiller NP, Privratsky JR, Zhang JJ, Reyes E, Wang D, Taylor GA, Gunn MD, Ko DC, Cook DN, Chandramohan V, Crowley SD and Hammer GE. (2021). Th17 immunity in the colon is controlled by two novel subsets of colon-specific mononuclear phagocytes. Frontiers in Immunology 12:661290. PMCID: PMC8113646
- Taylor GA, Huang HI, Fee BE, Youssef N, Jewell ML, Cantillana V, Schoenborn AA, Rogala AR, Buckley AF, Feng CG, Vallance BA, Gulati AS, Hammer GE. (2020) Irgm1-deficiency leads to myeloid dysfunction in colon lamina propria and susceptibility to the intestinal pathogen Citrobacter rodentium. PLoS Pathog 16(5):e1008553. PMCID: PMC7274479
- Liang J, Zhang JJ, Huang H, Kanayama M, Youssef N, Jin YJ, Reyes EY, Abram CL, Yang S, Lowell CA, Wang D, Shao L, Shinohara ML, Zhang JY, and Hammer GE. (2020). The ubiquitin-modifying enzyme A20 terminates C-type lectin receptor signals and is a suppressor of host defense against systemic fungal infection. Infect Immun Jun 15; doi:10.1128/IAI.00048-20. PMCID: PMC7440764
- Kanayama M, Makoto I, Danzaki K, Hammer G, He YW, Shinohara ML. (2015). Autophagy enhances NFkB activity in specific tissue macrophages by sequestering A20 to boost antifungal immunity. Nature Comm 6:5779. PMCID: PMC430441
- Liang J, Huang H, Benzatti F, Karlsson AB, Youssef N, Zhang JJ, Ma A, Hale LP and Hammer GE. (2016). Inflammatory Th1 and Th17 in intestine are each driven by functionally specialized dendritic cells with distinct requirements for MyD88. Cell Reports 17(5): 1330-1343. PMCID: PMC5123685
- Hammer GE, Turer EE, Taylor KE, Fang CJ, Advincula R, Oshima S, Barrera J, et al. (2011). Expression of A20 by dendritic cells preserves immune homeostasis and prevents colitis and spondyloarthritis. Nat Immunol 12(12):1184–1193. PMCID: PMC3419270
- Hammer GE, Gonzalez F, James E, Nolla H, and Shastri N. (2007). In the absence of aminopeptidase ERAAP, MHC class I molecules present many unstable and highly immunogenic peptides. Nat Immunol 8(1):101–108. PMID: 17128277