Postdoctoral Research Scientist
investigating the mechanism of antibody affinity maturation in germinal centres
Upon infection, activated B cells produce an immediate but short-lived antibody response. These antibodies tend to be weak with low affinity to their target antigens.
To create a most robust response activated B cells enter structures called germinal centres where they divide and mutate their antibody genes (the fantastically named process of somatic hypermutation). The cells then appear to compete to acquire antigen and for the attention of T follicular helper cells with only the best cells persisting. Through many cycles of testing this process ultimately produces antibodies of much higher affinity.
Equipped with these more powerful tools, B cells leaving the germinal centres produce a stronger response to infection and can persist as memory B cells in case the infectious agent is encountered again.
The mechanism by which germinal centre B cells compete is not completely understood. My project will test various models as to how germinal centres increase antibody affinity over time without compromising antibody diversity. In future this work could help design new vaccine methods designed to guide the immune system towards producing desired high affinity, neutralising antibodies, best for robust protection.
Prior to working at the Bannard group at the WIMM, I completed my PhD at the James lab at the University of Warwick investigating the localisation and signalling of the pre-T cell receptor.
Pre-T cell receptor localization and trafficking are independent of its signaling.
Smid AI. et al, (2023), J Cell Biol, 222
Systematic analysis of YFP traps reveals common mRNA/protein discordance in neural tissues.
Titlow JS. et al, (2023), J Cell Biol, 222
Systematic analysis of YFP gene traps reveals common discordance between mRNA and protein across the nervous system
Titlow J. et al, (2022)