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High-probability grants
According to our matching algorithm, Jonathan Yewdell is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2018 |
Yewdell, Jonathan W [⬀] |
ZIAActivity Code Description: Undocumented code - click on the grant title for more information. |
Immunobiology and Virology of Influenza a Virus @ Niaid Extramural Activities
Seasonal influenza imposes a significant socio-economic burden on humanity. Vaccination, the best hope for reducing the impact of influenza, is even under optimal circumstance effective in only 60% of individuals. The difficulty, of course, stems from the protean ability of influenza A virus (IAV) to rapidly escape existing immunity. IAV evolved an error prone polymerase that drives the rapid antigenic evolution of the two virion surface glycoproteins, neuraminidase (NA) and hemagglutinin (HA). Since the most potent antibodies (Abs) at neutralizing viral infectivity (neutralizing Abs, NAbs) are directed the head of the HA, amino acid substitutions in this region enable IAV to evade antibody (Ab)-based immunity. We are studying how IAV evolves under antibody pressure in vitro and in vivo, using ultra deep sequencing to detect mutations that reduce antibody affinity for IAV antigens and as well as epistatic alterations that mitigate fitness costs incurred by escape mutations. We are also studying the B cell response to IAV antigens, and have devised a novel approach that has enabled us for the first time to characterized the immunodominance hierarchy of antibody responses for distinct antigenic sites on the hemagglutinin glycoprotein.
|
0.914 |
2018 |
Yewdell, Jonathan W [⬀] |
ZIAActivity Code Description: Undocumented code - click on the grant title for more information. |
Translation in Immunity @ Niaid Extramural Activities
Class I molecules of the major histocompatibility complex (MHC) bind short peptides and present them to CD8+ T cells. CD8 positive T-cells play a critical role in eradicating intracellular pathogens (particularly viruses) and tumors. Nearly all viral peptides appear to derive from DRiPs (defective ribosomal products); rapidly degraded nascent proteins that fail to achieve a stable native conformation due to mistranslation, misfolding, mistargeting, or stoichiometric excess. We are characterizing all aspects of DRiP synthesis, degradation, and loading of DRiP-derived peptides onto class I molecules in the endoplasmic reticulum, the site of class I biogenesis. Following activation, lymphocytes can divide at dizzying rates (with cell cycles as rapid as 2 hr). We are studying the adaptions in translation that make this possible. Our findings suggest that the assumption that lymphocytes must synthesize all of the proteins required for division may not be true. Many other immune cells also demonstrate greatly increased translation following activation by viral infections or other insults. We are using a newly developed technique to study immune cell activation in tissue sections and also via flow cytometry, which has led to novel insights into immune cell function.
|
0.914 |