David J. Rawlings

This study shows that CD19 CAR-engineered regulatory T cells reduce B cell numbers, inflammation, and autoantibodies in lupus models, promoting long-term immune tolerance.

This study shows that lymphatic networks create spatially distinct environments in draining lymph nodes that influence B cell differentiation, affinity selection, and antibody isotype, which can be manipulated through vaccine design.

This study shows autoreactive B cells can initiate spontaneous germinal centers and autoimmunity through antibody-dependent mechanisms, independent of T cell interactions or antigen presentation.

The paper examines how RTS,S/AS01 vaccine induces transient protective B cell responses against malaria, which are later replaced by non-protective memory B cells, explaining its limited long-term efficacy.

This study develops a humanized mouse model to evaluate engineered plasma cells and their therapeutic antibody secretion, showing long-term antibody production and neutralization of SARS-CoV-2.

The paper identifies BCL6 and CD4+ T cell dependence in generating functional IgM+ memory B cells independent of germinal center formation.

The paper isolates PcrV-specific B cells from cystic fibrosis patients and generates monoclonal antibodies that reduce Pseudomonas aeruginosa burden in mice.

This study identifies SH2B3 as a critical regulator of T cell tolerance in T1D, showing that its deficiency enhances cytokine signaling and promotes islet destruction.

This study shows that increased PI3Kδ activity in Tregs disrupts their function and homeostasis, leading to immune dysregulation and autoimmunity in mice.

This study shows the IFIH1-A946T risk variant increases T1D risk in females but not males by enhancing IFN I signaling and altering immune cell profiles in NOD mice.

This study expands NHP B cells ex vivo, identifies unique plasma cell markers, and establishes AAV transduction conditions for engineered B cell therapies.

This study evaluates the efficacy of ssODN and rAAV6 donor templates in correcting sickle cell disease via ex vivo gene editing of HSCs, showing ssODN achieves higher in vivo gene correction.