- Select a language for the TTS:
- UK English Female
- UK English Male
- US English Female
- US English Male
- Australian Female
- Australian Male
- Language selected: (auto detect) - EN
Play all audios:
Re-exposure to antigen elicits a robust antibody response in serum, as well as inducing the formation of new ‘recall’ germinal centres (GCs) in lymphoid tissue. The serum antibody response
observed after antigen re-exposure is mainly driven by memory B cells, whereas the newly formed recall GCs are almost entirely composed of naive B cells. ‘Recall immunization’ is thus
specifically associated with an antibody response mediated by memory B cells that had been generated during the primary antigen encounter, as well as a de novo GC response. This may
counteract the phenomenon of ‘original antigenic sin’, in which the antibody response to a previously encountered pathogen can impair subsequent responses to closely related pathogens.
However, the mechanisms that facilitate the selective use of ‘primary-derived’ memory B cells for antibody production and the selective recruitment of naive B cells to recall GCs are not
well understood.
In a recent preprint (not peer-reviewed), Schiepers et al. show that the seemingly divergent antibody and GC responses observed in recall immunization are linked to antibody-mediated
feedback regulation. The authors immunized mice with recombinant haemagglutinin in the right hind footpad, and boosted these mice in the contralateral footpad with the same antigen 1 month
later. They found that B cells recruited to the recall GCs did not detectably bind antigen and were thus unable to contribute to antibody titres. The authors hypothesized that pre-existing
antibodies were suppressing the ability of B cells with antigen-binding capacity from entering recall GCs. To test this, they ablated plasma cell precursors in the primary GCs to deplete
circulating antibodies before homologous boosting. This significantly increased antigen binding in the new recall GCs. Boosting with variant antigens also increased antigen binding in recall
GCs, which suggests that antibody feedback steers recall GC B cells towards variant epitopes.
Anyone you share the following link with will be able to read this content:
