You are here

Gianna Hammer

Assistant Professor
Immunology
(919) 660-9003
Research Interest: 
Immunology
Signal transduction
Research Summary: 
Signaling pathways that govern how dendritic cells interact with microbial commensals in the intestine.
Research Description: 

The human intestine harbors an enormous amount of bacteria; remarkably, intestinal microorganisms outnumber host cells 10 to 1. To the immune system, co-existance (known as symbiosis) with these bacteria is a remarkable paradox: while immune cells are skilled operatives fixated on eliminating microbial invaders, these same cells are somehow restrained from attacking microbial symbionts. New insight into the immune system’s decision-making process of whether to attack or stay quiet has highlighted the role of dendritic cells: Specialized sentinels with unique ability to activate and shape immune responses. Because the immune system is exquisitely sensitive to the behavior of dendritic cells, perturbation of dendritic cell function or responses to bacteria that naturally live in the intestine can cause unwanted immune activation—resulting in autoimmune or inflammatory disease. My research goals are to identify molecules and signaling pathways that govern how dendritic cells interact with intestinal bacteria. Corruption of these processes can drive inflammatory bowel disease (IBD). I have identified one key pathway, regulated by the NF-κB attenuating enzyme A20 (Tnfaip3), which is required to maintain intestinal homeostasis and prevent IBD and IBD-associated arthritis. I seek to define signaling pathways that interact with A20 and determine how A20 regulates dendritic cell functions to establish host-commensal symbiosis. Conversely, I seek to define how corruption of dendritic cell functions, such as occurs in A20-deficient cells, induces intestinal inflammation and IBD.

Publications: 
Molecular control of steady-state dendritic cell maturation and immune homeostasis.
Hammer GE, Ma A.
Annu Rev Immunol. 2013. 31:743-91.

Dimerization and ubiquitin mediated recruitment of A20, a complex deubiquitinating enzyme.
Lu TT, Onizawa M, Hammer GE, Turer EE, Yin Q, Damko E, Agelidis A, Shifrin N, Advincula R, Barrera J, Malynn BA, Wu H, Ma A.
Immunity. 2013. 38:896-905.

Cutting edge: ABIN-1 protects against psoriasis by restricting MyD88 signals in dendritic cells.
Callahan JA, Hammer GE, Agelides A, Duong BH, Oshima S, North J, Advincula R, Shifrin N, Truong HA, Paw J, Barrera J, DeFranco A, Rosenblum MD, Malynn BA, Ma A.
J Immunol. 2013. 191:535-9.

Expression of A20 by dendritic cells preserves immune homeostasis and prevents colitis and spondyloarthritis.
Hammer GE, Turer EE, Taylor KE, Fang CJ, Advincula R, Oshima S, Barrera J, Huang EJ, Hou B, Malynn BA, Reizis B, DeFranco A, Criswell LA, Nakamura MC, Ma A.
Nat Immunol. 2011. 12:1184-93.

In the absence of aminopeptidase ERAAP, MHC class I molecules present many unstable and highly immunogenic peptides.
Hammer GE, Gonzalez F, James E, Nolla H, Shastri N.
Nat Immunol. 2007. 8:101-8.