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Activity 43.1 How Does the Immune System Keep the Body
Free of Pathogens?
Draw a Rube Goldberg cartoon-type diagram or develop a dynamic (claymation-type)
model to demonstrate how the components of the immune system interact to rid the body
of a pathogen—for example, a bacterial cell or a viral particle. Be sure to explain the
function of each “actor” in the system. Your diagram or model should include all the
terms below.
Here is an example of a Rube Goldberg–type drawing:
TERMS:
bacterium or virus
particle
helper T cell receptor
helper T cell
cytotoxic T cell
active cytotoxic T cell
macrophage
B cell
memory helper T cell
memory B cell
memory T cell
plasma cell
interleukins
(or cytokines)
CD4 protein
MHC molecules
antibody
antigen
epitope
thymus
bone marrow
hypothalamus
fever
clonal expansion
self versus nonself
After you have completed your model or diagram, use what you have learned to
answer the questions on the next page.
1. What are pathogens? Why do we need to prevent them from colonizing our bodies?
If pathogens do manage to colonize, what effects can they have?
Pathogen is a generic term for any disease-causing organism. Pathogens include
disease-causing bacteria, viruses, fungi, and protists.
The cells of our bodies contain all the components required for life. These components
support the lives of our own cells and can easily support the lives of pathogens, which
can compete with our own cells and potentially destroy them.
Pathogens can have the following effects:
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They overgrow and put pressure on specific membranes or cavities. When this
occurs in the ear, eardrums may rupture. When it occurs in the sinuses, the
pressure builds up to cause blockage and pain.
They produce toxins that can destroy our cells. For example, some strains of
bacteria produce exotoxins that can destroy cellular structure.
They parasitize cells and destroy their normal structure and function. Many fungal
infections—for example, athlete’s foot—are parasitic.
2. What general defense mechanisms does the body use to help prevent colonization by
pathogens? For example, what general defense mechanisms are involved in local
inflammatory responses?
The skin and mucous membranes act as physical barriers to the entry of pathogens.
In addition, glandular secretions include lysozymes and keep the skin at an acidic pH
(between 3 and 5), which inhibits the growth of many microbes.
A localized injury (for example, a cut or sliver) releases prostaglandins and histamines,
which cause increased blood flow and swelling in the area. The clotting mechanism helps
prevent invasion by additional pathogens. Phagocytic white blood cells move into the
region quickly and consume the pathogens to prevent their colonization. The pus that
forms at the site of an infection is an accumulation of these phagocytic cells. (Refer also
to pages 901–903 in Biology, 7th edition, for a more detailed description.)
3. In specific immunity, how do B cell responses differ from T cell responses?
B cell responses
T cell responses
Individual B cells respond to
specific types of foreign antigens
by secreting antibodies that interact
with the antigen and cause cells
with the antigen to agglutinate or
clump together. This agglutination
tags or identifies the antigens for
removal by phagocytic
macrophages. Other antibodies can
interfere with the function of
antigens by binding with them and
blocking their actions.
When body cells become infected with a pathogen,
a piece of foreign protein from the pathogen
interacts with an MHC molecule. (Cell infection
can occur by phagocytosis or by endocytosis.) The
MHC-antigen complex migrates to the surface of
the cell’s membrane. Individual T cells bearing
complementary antigen receptors on their
membrane surfaces interact or bind with the
antigen displayed on the MHC. Cytotoxic T cells
bind to foreign proteins displayed on class I MHC
molecules. Helper T cells bind to antigens
displayed on class II MHC molecules. Cytotoxic
T cells act directly by killing the infected cell.
Helper T cells respond by dividing and producing
a clone of activated helper T cells and memory
helper T cells. The activated helper T cells produce
cytokines (for example, interleukin-2), which help
the appropriate B cells to differentiate into
antibody-producing cells. They also help cytotoxic
T cells to become active in killing the infected
cells.
4. If about 105 genes are available in the human genome to produce proteins, how can we
produce more than 10  106 different kinds of Ab receptors (proteins) on B cells?
Although Biology, 7th edition, doesn’t explain this in any detail, the information that the
immune system can produce more types of B cells than there are genes in the genome
begs this question. Each of the variable regions of the antibody (on both light and heavy
chains) is made up of three parts. Each is coded by a different region on the DNA. The
DNA segments for the three separate parts of each variable region undergo random
recombination in the production of B cells. As a result, many fewer genes are required to
code for the 10  106 different kinds of Ab receptors (proteins) on B cells.
5. How does HIV affect the immune system?
HIV (human immunodeficiency virus) targets cells that display both the CD4 receptor
and a chemokine receptor. These two receptors are found on T helper cells. Infection by
HIV ultimately leads to the death of T helper cells and as a result destroys immune
responses triggered by T helper cells. Infected individuals cannot fight off infections and
may die.