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may not prevent an infection the first time a pathogen ap- Chapter 22 The Lymphatic System and Immunity 841
pears in the body. However, a person who survives the first
infection will probably be resistant to that pathogen in the Figure 22–25 The Course of the Body’s Response to a
future, thanks to a rapid and overwhelming secondary re- Bacterial Infection. The basic sequence of events begins with the
sponse. The effectiveness of the secondary response is one
of the basic principles behind the use of immunization to appearance of bacteria in peripheral tissues at time 0.
prevent disease.
Neutrophils Macrophages Plasma cells
&T i p s T r i c k s
The antibody response is like ordering a custom suit. The Number of active immune cells Natural Cytotoxic Antibody
first suit (the primary antibody response) takes time to make killer cells T cells level
because the tailor (an activated B cell) must first make a pat-
tern (a clone of memory cells). Subsequent suits (secondary 01 2 3
responses) are made much more quickly because the pattern Time (weeks)
already exists.
by a gradual, sustained increase in the activity (titer) of circulat-
Summary of the Immune Response
ing antibodies.
We have now examined the basic cellular and chemical inter-
actions that follow the appearance of a foreign antigen in the Figure 22–26 provides an integrated review of the rela-
body. Table 22–2 reviews the cells that participate in tissue de-
fenses and Figure 22–25 gives a timeline for their appearance at tionship between innate and adaptive immunity. The basic
the site of a bacterial infection.
sequence of events is similar when a viral infection occurs. The
In the early stages of infection, neutrophils and NK cells
migrate into the threatened area and destroy bacteria. Over initial steps are different, however, because cytotoxic T cells
time, cytokines draw increasing numbers of phagocytes into the
region. Cytotoxic T cells appear as arriving T cells are activated provide an adaptive defense and NK cells provide an innate
by antigen presentation. Last of all, the population of plasma
cells rises as activated B cells differentiate. This rise is followed defense. Figure 22–27 contrasts the events involved in defend-
ing against bacterial infection with those involved in defending 22
against viral infection.
Table 22–2 Cells That Participate in Tissue Defenses
Cell Functions
Neutrophils Phagocytosis; stimulation of inflammation
Eosinophils Phagocytosis of antigen–antibody complexes; suppression of inflammation; participation in allergic
response
Mast cells and basophils Stimulation and coordination of inflammation by release of histamine, heparin, leukotrienes,
prostaglandins
Antigen-Presenting Cells
Macrophages (free and fixed macrophages, Phagocytosis; antigen processing; antigen presentation with Class II MHC proteins; secretion
Kupffer cells, microglia, etc.) of cytokines, especially interleukins and interferons
Dendritic cells Pinocytosis; antigen processing; antigen presentation bound to Class II MHC proteins
Lymphocytes
NK cells Destruction of plasma membranes containing abnormal antigens
Cytotoxic T cells (TC, CD8 marker) Lysis of plasma membranes containing antigens bound to Class I MHC proteins; secretion of perforins,
defensins, lymphotoxins, and other cytokines
Helper T cells (TH, CD4 marker) Secretion of cytokines that stimulate cell-mediated and antibody-mediated immunity; activation
of sensitized B cells
B cells Differentiation into plasma cells, which secrete antibodies and provide antibody-mediated immunity
Suppressor T cells (TS, CD8 marker) Secretion of suppression factors that inhibit the immune response
Memory cells (TS, TH, B) Produced during the activation of T cells and B cells; remain in tissues awaiting rearrival of antigens

