Page 853 - Fundamentals of anatomy physiology
P. 853
840 Unit 4 Fluids and Transport
Primary and Secondary Responses Activated B cells start dividing immediately. At each cycle
to Antigen Exposure of division, some of the daughter cells differentiate into plasma
cells, while others continue to divide. Molecules of immuno-
The initial immune response to an antigen is called the pri- globulin M, or IgM, are the first to appear in the bloodstream.
mary response. When the antigen appears again, it triggers The plasma cells that produce IgM differentiate after only a few
a more extensive and prolonged secondary response. This cycles of B cell division. Levels of immunoglobulin G, or IgG, rise
response is due to the presence of large numbers of memory more slowly, because the plasma cells responsible differenti-
cells that are primed for the arrival of the antigen. Primary and ate only after repeated cell divisions that also generate large
secondary responses occur in both cell-mediated and antibody- numbers of memory B cells. In general, IgM is less effective
mediated immunities. Let’s look at the pattern of antibody pro- as a defense than IgG. However, IgM provides an immediate
duction over time to see the differences between the primary defense that can fight the infection until massive quantities of
and secondary responses. IgG can be produced.
22 The Primary Response The Secondary Response
The primary response takes time to develop because the anti- Unless memory B cells are exposed to the same antigen a second
gen must activate the appropriate B cells. These cells must then time, they do not differentiate into plasma cells. If and when
differentiate into plasma cells. As plasma cells differentiate that exposure occurs, the memory B cells respond right away—
and begin secreting, the concentration of circulating antibodies faster than the B cells stimulated during the initial exposure.
makes a gradual, sustained rise (Figure 22–24a). This response is immediate in part because memory B cells are
activated at relatively low antigen concentrations. In addition,
During the primary response, the antibody titer, or level these cells synthesize more effective and destructive antibodies.
of antibodies in the plasma, does not peak until one to two Activated memory B cells divide and differentiate into plasma
weeks after the initial exposure. If the individual is no lon- cells that secrete these antibodies in massive quantities. This
ger exposed to the antigen, the antibody concentration then secretion is the secondary response to antigen exposure.
declines. The antibody titer declines because (1) plasma cells
have very high metabolic rates and survive for only a short During the secondary response, antibody concentrations
time, and (2) suppressor T cells release suppression factors that and titers increase more rapidly and reach levels many times
inhibit further production of plasma cells. However, suppres- higher than they did in the primary response (Figure 22–24b).
sor T cell activity does not begin immediately after exposure The secondary response appears even if the second exposure
to the antigen. Also, under normal conditions helper T cells occurs years after the first. The reason is that memory cells may
outnumber suppressor T cells by more than 3 to 1. As a result, survive for 20 years or more.
many B cells are activated before suppressor T cell activity has
a noticeable effect. The primary response develops slowly and does not pro-
duce antibodies in massive quantities. For these reasons, it
Figure 22–24 The Primary and Secondary Responses in Antibody-Mediated Immunity.
PRIMARY SECONDARY
RESPONSE RESPONSE
Antibody level IgG
in plasma
IgG IgM
IgM
1234
1234 Time (weeks)
Time (weeks)
b The secondary response has a very rapid increase in IgG antibody
a The primary response takes about two weeks to develop concentration and rises to levels much higher than those of the
peak antibody levels (titers). IgM and IgG antibody levels primary response. Antibody levels remain elevated for an
do not remain elevated. extended period after the second exposure to the antigen.

