How a specific immune signal boosts antibody killing of virus-infected cells
The Unexpected Role of TNFRSF14 Signaling in Promoting Antibody-Dependent Cell-Mediated Cytotoxicity
Looks at whether a particular immune signal helps antibodies recruit immune cells to kill herpes-infected cells and protect people from herpes simplex.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Albert Einstein College of Medicine NIH-funded |
| Lab location | 1 site (Bronx, United States) |
| Project ID | NIH-11228767 on NIH RePORTER |
What this research studies
Researchers created a weakened, single-cycle herpes simplex virus (∆gD-2) vaccine that cannot spread and found it protects mice by making antibodies that call in immune cells to kill infected cells (ADCC) rather than by neutralizing the virus. They isolated a protective monoclonal antibody called BMPC-23, showed it works in mice and in models with human Fc receptors, and used cryo-electron microscopy to map where the antibody binds on the virus protein. The project focuses on the role of TNFRSF14 signaling in promoting this antibody-dependent cell-mediated cytotoxicity. Work combines animal experiments, antibody isolation and structural mapping to understand and strengthen this immune-killing pathway.
Who could benefit from this research
Good fit: Adults with recurrent herpes simplex infection or people at high risk of HSV exposure would be the most relevant candidates for future trials or participation.
Not a fit: People with severely weakened immune systems who cannot carry out antibody-dependent cellular killing or those with unrelated medical issues may not benefit from this approach.
Why it matters
Potential benefit: If successful, this work could lead to vaccines or antibody therapies that protect people from herpes simplex by boosting immune cell–mediated killing rather than relying only on neutralizing antibodies.
How similar studies have performed: Preclinical animal studies of the ∆gD-2 vaccine and the BMPC-23 antibody showed protection through ADCC, but translating this success to humans has not yet been done.
Where this research is happening
Bronx, United States
- Albert Einstein College of Medicine — Bronx, United States (Active)
Researchers
- Principal investigator: Herold, Betsy C. — Albert Einstein College of Medicine
- Study coordinator: Herold, Betsy C.
About this research
- This is an active NIH-funded research project — typically early-stage science, not a clinical trial accepting patient enrollment.
- Some NIH-funded labs run parallel clinical studies or seek volunteers for related work. To check, contact the principal investigator or institution listed above.
- For full project details, budget, and progress reports, visit the official NIH RePORTER page below.