top of page
UPDATED The Barber Lab Logo (no bkgrd).p

Glen N. Barber, PhD, FRS

Chairman and Professor

Department Cell Biology

Eugenia J. Dodson Chair in Cancer Research

University of Miami Miller School of Medicine

Picture30.png
Barber_final.jpg

                       Barber Lab News 

Our laboratory is interested in studying mechanisms of host defense against microbes and cancer. Through these efforts, our laboratory and others have discovered how our cells in our body recognizes microbial infection to trigger host defense responses. This process is controlled by cellular sensors which recognize microbe-specific molecules which elicit an innate immune signaling cascade leading to the transcription of key genes such as type I interferon (IFN) and cytokines that stimulate adaptive immunity. While essential for host defense countermeasures, such cellular innate immune signaling pathways can also cause inflammation, if overstimulated. Thus, innate immune signaling process are carefully controlled, to avoid chronic cytokine production. Innate immune signaling is also essential for the effective generation of anti-tumor adaptive immunity. Understanding these mechanisms has shed considerable insight into pathogenesis and has led to the development of novel therapeutics to treat a variety of infectious, inflammatory and cancer related disease. Our laboratory continues to study these processes.

Sting Signaling

  • Contributions to unraveling mechanisms of innate immune signaling...read more

  • Discovery of the STING, cytosolic DNA activated innate immune pathway...read more

                                          Barber Lab Highlights 
                     

                             How tumor cells avoid the immune system
 

                                                       Featured Publication


Extrinsic Phagocyte-Dependent STING Signaling Dictates the Immunogenicity of Dying Cells.
                                                                                      Ahn et al., Cancer Cell 2018 
 



.
 

bottom of page