Our Focus

Our laboratory specializes in studying immune escape in viruses and cancers, as well as designing, identifying and engineering novel antibodies that can overcome such escape signatures. Our current work focuses on HIV-1 and B-cell lymphomas. In both areas, we combine human immunology, antibody engineering and translational models to move from mechanisms to molecules, providing meaningful preclinical proof. Our overall aim is to rapidly translate our findings into clinical applications.

The main focus of our HIV program is on broadly neutralizing antibodies (bNAbs) and their potential use in novel therapeutic strategies for treating, preventing, and potentially curing HIV-1 infections. To this end, we are developing novel, antibody-based treatment approaches. We are engineering highly potent, multispecific antibodies and investigating HIV-1 antibody resistance in people living with HIV (PLWH). Our approach combines longitudinal patient cohorts, single-B-cell discovery, antibody engineering, and translational in vivo models to advance immunotherapy against HIV-1.

What we do:

• Discover and profile bNAbs using single-cell cloning, high-throughput neutralization on diverse viral panels, and escape mapping to reveal conserved vulnerabilities in the HIV envelope.
• Dissect viral escape from bNAbs by developing novel assays to rapidly profile resistance directly in people living with HIV (PLWH). Integrate paired genotype-phenotype datasets to enable individualized, in silico bNAb response prediction.
• Model real-world pressure using viral fitness/escape landscapes, synergy testing of antibody (Ab) combinations versus multispecifics, and resistance forecasting to prioritize robust antibody (combination) leads.
• Evaluate prevention and therapy candidates in advanced humanized mouse models to select candidates for future clinical development.

Why it matters

Our goal is to improve future bNAb treatment, prevention and cure approaches by matching the right antibody (or combination) to the right individual. To achieve this, we aim to discover potent bNAbs, measure resistance directly in PLWH, and integrate paired genotype–phenotype data into in silico prediction. Furthermore, our novel multispecific bNAbs may be broad and potent enough to overcome common HIV-1 antibody escape signatures, eliminating the need to pre-screen PLWH for antibody sensitivities. Thus, our goals are to improve future HIV-1 antibody therapies by matching the right bNAb to the right PLWH and to engineer novel antibody formats that could be used universally on a global scale to treat, prevent, and/or cure HIV-1 infections.

We aim to improve and advance lymphoma immunotherapies using our deep knowledge of antibody design and engineering. Although current bispecific antibodies targeting CD3 and CD20 show promise in treating aggressive lymphomas, real-world use reveals important limitations, such as relapse, resistance, and cytokine release syndrome. To address these limitations, we plan to use multispecific antibodies (msAbs) that target multiple antigens, enabling more precise targeting of lymphomas, specific immune cell subsets, and different immune cell compartments simultaneously. Our ultimate goal is to design molecules that attack tumors from multiple angles, thereby limiting and overcoming immune escape, and converting that design power into new therapeutic options.

What we do:

• Map escape routes by defining how lymphomas evade immune engagement and therapy over time, turning those liabilities into actionable design rules.
• Our multispecifics platform uses a modular toolkit that combines complementary antigen recognition with tailored effector engagement. This toolkit rapidly iterates architectures to balance potency, selectivity, and safety.
• Translate and de-risk by advancing lead multispecific antibodies through stepwise evaluation in novel ex vivo systems and in vivo lymphoma models to prioritize candidates for future clinical development.

Why it matters

Single-path approaches leave room for escape. Multispecific antibodies narrow these exits by combining multiple recognition and immune activation strategies into one molecule. This aims to achieve deeper, more durable responses in aggressive lymphomas while maintaining a clear path to the clinic.