We investigate how B cells interpret mechanical cues through Piezo1 to fine-tune antigen discrimination and maintain self-tolerance. By understanding how different physical contexts shape B cell fate and immune output, this research seeks to reveal novel regulatory mechanisms that can be leveraged to prevent autoimmunity. 

The actin cytoskeleton plays a pivotal role in organizing the immune synapse and modulating signaling sensitivity. We study how cytoskeletal regulatory factors at the B cell synapse adjust activation thresholds, safeguard self-tolerance, and ultimately influence the magnitude and quality of immune responses. 

High antigen valency is a potent driver of B cell activation and a fundamental principle in vaccine design. We explore how B cells sense and respond to multivalent antigens at molecular and cellular levels, aiming to uncover evolutionary adaptations that favor breaking tolerance against viral epitope displays. Insights gained will inform strategies to harness or control this process in vaccine development.

Affinity maturation in germinal centers is critical for producing high-quality antibodies. We study how germinal center B cells undergo intrinsic preparatory changes to favor the selection of clones with superior antigen affinity. This work seeks to uncover additional intrinsic mechanisms that guide optimal clonal selection during the germinal center reaction. 

B cells adapt to a wide array of environmental inputs to achieve optimal immune protection. However, novel or persistent environmental stimuli in modern settings can inadvertently disrupt tolerance and trigger B cell mediated pathologies. We aim to define the molecular and cellular mechanisms by which such external cues recalibrate B cell activation and contribute to the development of immune mediated diseases. 

BAFF(B cell activating factor) is a key driver of B cell survival and differentiation, and elevated BAFF levels are linked to multiple autoimmune disorders. We investigate how BAFF overabundance reprograms B cell characteristics in ways that promote loss of tolerance, seeking to define critical yet unexplored mechanisms underlying its pathogenic potential. 

We aim to identify predictive markers for the generation of long-lived plasma cells in the context of vaccination. By linking vaccine-induced B cell differentiation patterns to the durability of antibody responses, this work supports the rational design of immunization strategies that confer sustained protection. 

Systemic lupus erythematosus (SLE) is characterized by autoantibody production and widespread inflammation. We focus on the signaling networks that amplify immune activation during disease flare-ups, with particular attention to how pro-inflammatory mediators reshape immune cell behavior and escalate pathology. 

We are developing a minimally invasive microneedle-based system for delivering human papillomavirus vaccines. This platform is designed to induce robust systemic immunity while enabling needle-free, cold chain–independent administration, offering scalable solutions for both high-resource and resource-limited settings. 

Our team develops integrated in vitro and in vivo platforms to assess vaccine efficacy. These systems combine surrogate viral neutralization assays with real-time monitoring of protective antibody activity in animal models, enabling comprehensive evaluation from early discovery to preclinical validation.