SARS-CoV-2 reinfection has been observed among some previously infected individuals, raising the possibility that infection-induced immunity against SARS-CoV-2 may be short-lived, as is the case for seasonal coronaviruses 22, 23, 24, 25, 26, 27, 28.
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While SARS-CoV-2 infection induces a durable B cell response, antibody levels decay over time, raising the risk that immunity may wane as the neutralizing antibody titre decreases below the threshold needed to protect against reinfection 17, 18, 19, 20, 21. The quality of the B cell response following severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection determines the duration and breadth of protective immunity. In this manner, memory B cells and plasma cells cooperate to provide overlapping layers of protection against reinfection by the pathogen or related variants. Plasma cells persist in sites such as the bone marrow and serve as a first line of defence against pathogen reinfection through constitutive secretion of antibodies 14, 15, 16. By contrast, plasma cells are a terminally differentiated population of cells that tend to be specific for the subtype of virus previously encountered. The reduced mutational load of memory B cells could facilitate their ability to recognize and respond to viral variants, with the memory B cell population in humans containing clones that are broadly reactive to several pathogens, including influenza virus and HIV 12, 13. Following antigen re-encounter, memory B cells can also re-enter the GC, where they undergo further affinity maturation 11. Memory B cells persist for years to decades and rapidly differentiate into antibody-secreting cells upon antigen re-encounter 10, 11.
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B cells that accrue productive mutations within their B cell receptor preferentially capture and present antigens to T cells upon their return to the light zone, facilitating their eventual differentiation into memory B cells or plasma cells 2, 5, 6.ĭata generated in mouse models suggest that memory B cells tend to emerge from the GC before plasma cells and, accordingly, display reduced levels of somatic hypermutation 7, 8, 9. The magnitude of T cell help received by a B cell in the light zone dictates the extent of cell division and somatic hypermutation that occurs within the dark zone 3, 4. Within the GC, B cells compete for a limiting amount of T cell-derived signals, such as cytokines and CD40 ligand, that promote their migration from the light zone to the dark zone 2.
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During an immune response, B cells that encounter their cognate antigen become activated and migrate to the centre of the B cell follicle, where they form structures known as germinal centres (GCs) 1.