An antigen to remember: regulation of B cell memory in health and disease.
Vaccine success relies on the formation of immunity. Humoral immunity is critical and is mediated by long-lived antibody-secreting cells and memory B cells (MBCs). Chronic infectious diseases cause a significant global burden of disease; pathogens that evade the immune system can cause phenotypical and functional changes to immune memory populations. Thus, recent studies have focused on MBC subset function. IgM+MBCs have emerged as important early responders in malaria. Atypical MBCs have functional qualities associated with exhaustion in chronic infectious diseases, but the requirements for their formation and where they localize remains unknown. Similarly, the T-bet-driven transcriptional program drives formation of MBCs phenotypically similar to atypical MBCs. Identifying protective or detrimental roles of MBC subsets, and their regulators, will be important for clinical intervention.
Infection and Immunity Program and The Department of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria 3800, Australia.
Aleta
A
Pupovac
Infection and Immunity Program and The Department of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria 3800, Australia. Electronic address: kim.jacobson@monash.edu.
Kim L
KL
Good-Jacobson
D000818:Animals; D001402:B-Lymphocytes / Q000276:immunology* / Q000473:pathology; D002908:Chronic Disease; D006801:Humans; D007075:Immunoglobulin M / Q000276:immunology*; D007156:Immunologic Memory; D007239:Infections / Q000276:immunology* / Q000473:pathology; D020825:T-Box Domain Proteins / Q000276:immunology*; D000098815:T-bet Transcription Factor
D007075:Immunoglobulin M; D020825:T-Box Domain Proteins; D000098815:T-bet Transcription Factor