IVRI Faculty director publishes new potential target for immunotherapy – The activation of the adaptor protein STING depends on its interactions with the phospholipid PI4P
UC Berkeley Assistant Professor in Immunology Michel DuPage published in Cancer Immunology – Separating the Good from the Bad: Tumor-Infiltrating Tregs Have Increased Fucosylation
IVRI faculty director David Raulet and collaborators, reviewed in Nature Reviews Immunology, why Natural killer (NK) cells are emerging as important new additions to the cancer therapeutic arsenal.
IVRI faculty Dr. Vance and his team develop the first oral infection mouse model for Shigella infection that recapitulates human disease.
IVRI investigator Russell Vance and his team show, in a paper published in Nature Communications, evidence that ancestral interferon-independent functions of STING mediate antiviral responses in vivo
Dr. Winoto’s team new study, supported by IVRI and Aduro Biotech (grant #043572), demonstrates a novel approach that leads to effective T‐cell responses against tumors in mice with potential future applications in humans.
IVRI faculty director, David Raulet, comments in this week Science edition, a publication by Zhou et al. showing that, cytotoxic lymphocytes both kill target cells and activate additional inflammatory signals through pyroptosis.
Dan Fletcher’s lab reveals how a viral pathogen hijacks branched actin network assembly to drive cell-cell fusion; a mechanism essential for tissue development and used by some viruses to form pathological syncytia.
IVRI is proud to feature “Fab” article from UC Berkeley Pr. Jay Groves. Understanding how T Cell receptors (TCRs) are activated is fundamental in the cancer immunotherapy field. The present study is probably the first to put a quantitative measure on specific potency of a synthetic TCR ligand, and identifies the specific H57-Fab’ epitope as a potent target; both of these insights being essential in drug development.
IVRI faculty Prof. Greg Barton recently demonstrated the importance of the location of Toll-like-receptors (TLRs). In a new study published in PNAS, Alison Stanbery, Zachary Newman, and Prof. Gregory Barton show that not only location of TLR-9 is primordial, but dysregulated activation of TLR-9 at different stages of life, induced specific inflammatory response. This work helps us understand unique aspects of TLR9-driven inflammatory disease, and has relevance for studying and developing new therapeutic avenues for both infectious and autoimmune diseases.