The secondary immune response is more rapid and intense due to the presence of memory cells created during the primary response.

After an infection is cleared, most of the activated lymphocytes undergo apoptosis to prevent excessive immune activity.

Dendritic cells are the most effective antigen-presenting cells and play a critical role in activating T-cells.

Memory T-cells remain in the body after an infection and respond faster upon re-exposure to the same antigen.

B-cells differentiate into plasma cells that produce antibodies to target specific antigens.

MHC Class II molecules present antigens derived from extracellular pathogens via the exogenous pathway to helper T-cells.

Immunological memory allows the immune system to respond more rapidly and effectively to previously encountered antigens.

Memory B-cells and T-cells remain in the body after an infection and respond rapidly and robustly if the same pathogen is encountered again.

Cytokines are signaling molecules that help regulate immune cell behavior, including differentiation, proliferation, and activation.

MHC molecules present antigen fragments on cell surfaces for recognition by T-cells, crucial for adaptive immunity.

The adaptive immune response begins with antigen recognition by antigen-presenting cells, which then activate lymphocytes.

MHC Class I molecules present antigens from within infected cells to cytotoxic T-cells (CD8+), initiating their response.

Regulatory T-cells help maintain immune tolerance and prevent autoimmunity by suppressing excessive immune responses.

MHC molecules display antigen fragments on the surface of cells to be recognized by T-cells, crucial for initiating an adaptive immune response.

The immune synapse is a structure that forms between a T-cell and an antigen-presenting cell to facilitate cell signaling and T-cell activation.