immunological memory

Function

• a mechanism to protect us against reinfection

Pathology

• memory B-cells against SARS-CoV2 spike protein increase between 1 & 8 months after Covid-19 infection
  • IgG type most common memory B-cell with lesser IgA type
• memory T-cells CD4(+) & CD8(+) decline after Covid-19 infection with a 1/2life of 3-5 months (though the role of CD4(+) T-cells may occur largely within germinal centers)
• two mRNA vaccinations induce memory B-cells & T-cells that when stimulated by infection with SARS CoV2 alpha, beta or delta variants, produced neutralizing antibodies against those variants
  • CD4+ & CD8+ memory T-cells produced
  • memory B-cells & T-cells remained at high levels for at least 6 months

Physiology

• naive B-cells interact with T-cells in the presence antigens presented to T-cells by dendritic cells within lymphoid tissue to become activated B-cells
• the activated B-cells form germinal centers, proliferate & change antibody class & transform into early plasmablasts producing low-affinity antibody (IgM)
• some of the proliferating activated B-cells will become memory B-cells
• within the germinal center iterative cycles of proliferation, mutation & selection result in affinity maturation with increased antigen affinity of B-cell receptors
• throughout this response, some B-cells will differentiate into short-lived plasmablasts, long-lived plasmablasts & memory B-cells.
• upon recall, if plasma cell-derived antibodies are insufficient for protection, memory B-cell at all phases of development can rapidly differentiate into plasmablasts or initiate secondary germinal center responses in conjuction with follicular helper memory T-cells
• B-cell mutation & selection in the germinal center provides a mechanism to counteract pathogen mutation
• long-lived plasma cells produced in the germinal center response live in the gut, spleen, & bone marrow where they can survive for years to decades, continuously secreting antibodies independent of pathogen presence
  • circulating antibodies will be protective as long as the amount is sufficient to neutralize a pathogen inoculum
• in contrast to plasma cells, memory B-cells recirculate throughout the body & can be rapidly activated following reinfection to produce antibody-secreting plasmablasts or initiate secondary germinal center responses
• memory B-cells can respond to variants because they have a broader spectrum of affinity than is present in the antibodies secreted in response to the initial infection
• secondary germinal center responses drive production of new high-affinity antibody- producing plasmablasts specific to the new challenge
• emerging Covid-19 variants remain susceptible to memory T-cell responses
• follicular helper memory T-cells also enhance secondary antibody response
  • the T-cells recognize pathogen protein determinants mostly distinct from the antibody recognition site
• distinct recognition by B-cells & helper T-cells of the same pathogen promotes breadth & flexibility, & provides a check on inappropriate immune responses
• immune memory blocks future infections either by continued production of neutralizing antibodies from long-lived plasma cells or by recalling memory B-cells & memory T-cells to rapidly produce new plasmablasts & thus restore high-affinity, neutralizing antibodies in circulation.

More general terms

• memory

Additional terms

• memory B lymphocyte

Patient information

immunological memory patient information