Updated: 3/6/2018

Memory

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Overview
 

 
Introduction
  • The adaptive immune system maintains memory of past infections so that
    • the body is able to maintain a small number of primed cells
    • future (secondary) exposure to the same pathogen will be more robust because
      • adaptive immunity can be activated more quickly
      • memory cells can proliferate to higher levels
      • specific antibodies have undergone affinity maturation
  • Primary and secondary responses to pathogens differ in notable ways
Differences between Primary and Secondary Responses
Feature Primary Responses
Secondary Responses
Activation
  • Response must be activated by antigen presenting cells
  • Response can be generated directly through reactivation of memory cells
Response time
  • Response peaks in 5-10 days after infection
  • Response peaks in 1-3 days after infection
Peak response
  • Lower peak levels of adaptive immune cells
  • Higher peak levels of adaptive immune cells
Secreted proteins
  • First IgM then later IgG antibodies
  • Low affinity immunoglobulins
  • Fully differentiated IgG, IgA, and IgE antibodies
  • High affinity immunoglobulins
 
Memory B-Lymphocytes
  • Memory B-cells are a distinct population that 
    • have undergone isotype switching such that
      • memory B-cells express IgA, IgE, and IgG on surface
      • naive B-cells express IgM and IgD on surface
    • have enter resting cell stage
    • have dramatically increased affinity for antigen
  •  Activation of memory B-cells by antigens promotes
    • differentiation of B-cells into plasma cells
    • secretion of large quantities of antibodies
Memory T-Lymphocytes
  • Memory T-cells are different from primary T-cells because
    • they have decreased IL-2 receptors compared with effector T cells
    • they can remain dormant for years
    • they can be activated and induced to proliferate upon antigen exposure
  • Memory T-cells can also survive activation induced cell death (AICD) that involves
    • repression of T-cell function following an immune stimulus mediated by
      • Fas and Fas ligand death domain interactions
      • other cell-to-cell contacts
    • apoptosis of the T-cell population specific for an antigen
    • retention of a memory population after killing the effector T-cell population

References

 

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