Figure 1.

Immune response to infection and vaccination. Viral proteins are taken up by antigen presenting cells (APCs) that generate a range of pro-inflammatory cytokines. The antigens are presented to naive T cells that differentiate into different types of cells. T follicular helper (T_FH) cells assist B cells to differentiate into plasma cells that produce antigen-specific antibodies to neutralize the virus. A broad range of antibodies are generated against multiple epitopes on the spike protein, but those directed against the highly immunogenic receptor-binding domain appear to have the greatest neutralizing potential because they disrupt the interaction between the spike protein and the angiotensin II converting enzyme 2 receptor. Effector T cells destroy virus-infected cells. Macrophages phagocytose and digest antibody-tagged virus and virus-infected cells. Antigen-specific memory B and T cells develop to prevent future infection. In parallel with the serological response, antigen-specific memory B cells continuously acquire somatic mutations in their variable region genes to improve antigenic affinity. Upon antigenic reexposure, memory B cells drive the recall response by differentiating into high-affinity antibody-secreting plasma cells. Although antibody levels wane, antigen-specific memory B cells progressively become more numerous and mature.