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