Human Physiology, 14th edition (2016)

512 Chapter 15

the foreign antigen-MHC class-1 complex also stimulates pro-

liferation of those killer T cells. In addition, proliferation of the

killer T lymphocytes is stimulated by interleukin-2 secreted by

the helper T lymphocytes that were activated by macrophages

or dendritic cells ( fig. 15.17 ).

The network of interactions among the different cell types

of the immune system now spread outward. Helper T cells can

also promote the humoral immune response of B cells. It may

be recalled that B cell genes for antibodies undergo somatic

hypermutation and class switch recombination (section 15.2)

within the germinal centers of lymph nodes. The ability of B

cells to produce class-switched antibodies (from IgM to IgG,

IgA, or IgE) with a high affinity for their antigens depends on

helper T lymphocytes. These helper T cells home to the ger-

minal centers of lymph nodes where they may be activated by

antigen-presenting cells ( fig. 15.18 ). There, they aid B cells to

divide and develop into plasma cells and memory B cells. This

interaction between helper T cells and B cells helps provide

for long-term humoral immunity and the ability of vaccines to

evoke active immunity.

Destruction of T Lymphocytes

The activated T lymphocytes must be destroyed after the infec-

tion has been cleared. This occurs because T cells produce a

surface receptor called FAS. Production of FAS increases

T Lymphocyte Response to a Virus

Infection by a virus stimulates innate immune mechanisms at
the beginning of the infection. Antigen-presenting cells (mainly
dendritic cells and macrophages) have pathogen-recognition
receptors (PRRs) that cause these cells to engulf the viruses
and migrate to secondary lymphoid organs. Once there, they
present viral polypeptides together with MHC class-2 mol-
ecules to helper T lymphocytes. This activates the helper T cells
( fig.  15.15 ) to the viral antigens and changes them into effec-
tive T H 1,  T H 2, and the other specialized helper T cells previ-
ously discussed. These activated helper T cells are needed to
stimulate B cells to form memory cells and antibody-producing
plasma cells, and they also aid the proliferation of killer (cyto-
toxic) T lymphocytes. In short, the activation of helper T cells
is required for an optimal adaptive immune response by both
B and T lymphocytes to the viral infection.
Killer T cells can destroy infected cells only if those cells
display the foreign antigen together with their class-1 MHC
molecules ( fig.  15.16 ). Such interaction of killer T cells with

Figure 15.15 Interactions between antigen-
presenting cells, T cells, and B cells. (1) An antigen-
presenting cell presents a foreign antigen bound to a class-2
MHC molecule on its surface to a helper T cell. The T cell
receptor requires that the antigen be presented in this way in
order for the T cell to become activated. (2) Once activated,
the helper T cell is here interacting with a B cell to improve the
immune response to the foreign antigen.

Helper T

cells

Class-2 MHC

molecule

CD4 coreceptor

Foreign

antigen

Antigen-presenting cell

B cell

Activated

helper T cell

Foreign
particle

1

2

Figure 15.16 A killer T cell destroys an infected

cell. In order for a killer T cell to destroy a cell infected with

viruses, the T cell must interact with both the foreign antigen and

the class-1 MHC molecule on the surface of the infected cell.

Tissue cell

infected with

viruses

Viral antigen

Class-1 MHC molecule

CD8 coreceptor

Killer T cell

Destruction of

infected cell

Target cell