FIGURE 14.5 • Schematic diagram of the molecular interactions that occur during antigen presentation. To become activated, both cytotoxic and helper T lymphocytes need to identify presented antigens as “nonself” as well as recognize the appropriate class of MHC molecules. Note that each interaction between an antigen–MHC complex with its specific T-cell receptor (TCR) requires a costimulatory signal from the interaction of CD28 with B7 molecules. Without a costimulatory signal, the T cell cannot be fully activated. a. In all nucleated cells of the body, viral antigen or cancer (tumor-specific) proteins are displayed in the context of MHC I molecules to interact with cytotoxic CD8 T lymphocytes. b. On antigen-presenting cells (e.g., macrophages), the foreign antigen is displayed in the context of MHC II molecules to interact with a helper CD4 T lymphocyte.
FIGURE 14.6 • Schematic diagram of B lymphocyte activation leading to plasma cell and B memory cell formation.
B cells are activated by the binding of antigen (Ag) to B-cell receptors (BCRs; membrane-bound antibodies) expressed on their surface. As an antigen-presenting cell, a B cell internalizes the BCR–antigen complex, partially digests the antigen, and then displays parts of it on the surface of its own MHC II molecules. The T-cell receptor (TCR) on a helper CD4 T lymphocyte (TH2 cell) recognizes both the antigen and the MHC II molecule, activating the helper CD4 T lymphocyte. The activated helper CD4 T lymphocyte releases interleukins IL-2, IL-4, IL-5, IL-10, and IL-13, which promote division and differentiation of the B lymphocyte into plasma cells and memory B cells. Note the presence of a costimulatory molecule complex between the B and T cells. Ab, antibody.
FIGURE 14.7 • Schematic diagram of activation of natural killer cells leading to destruction of a transformed tumor cell by antibody-dependent, cell-mediated cytotoxicity (ADCC). The ADCC reaction involves (1) activation of natural killer (NK) cells by the binding of interferon  (IFN-), the powerful NK cell activator, to its cell surface receptor (IFNreceptor) and (2) the binding of an antibodyor an antibodyand complement-coated target cell to an NK cell bearing Fc receptors. These reactions induce apoptosis, or lysis, of the target cell, usually through the action of tumor-specific antibodies or the action of perforins and granzymes (fragmentins) secreted by activated NK cells.
Activated B lymphocytes differentiate into plasma cells and memory B cells.  Plasma cells synthesize and secrete a specific antibody.
During this process, activated B cells switch from synthe sizing their BCRs as integral membrane proteins to form ing a soluble version, which are called antibodies.  Memory B cells respond more quickly to the next encounter with the same antigen.
The specific antibody produced by the plasma cell binds to the stimulating antigen, forming an antigen–antibody complex. These complexes are eliminated in a variety of ways, including destruction by NK cells and phagocytosis by macrophages and eosinophils.
In antibody-dependent cell-mediated cytotoxicity (ADCC), IgG molecules direct NK cells to their target.