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Unit 1:
Ch. 1
Ch. 2
Ch. 3
Interlude A
Unit 2:
Ch. 4
Ch. 5
Ch. 6
Ch. 7
Ch. 8
Ch. 9
Interlude B
Unit 3:
Ch. 10
Ch. 11
Ch. 12
Ch. 13
Ch. 14
Ch. 15
Interlude C
Unit 4:
Ch. 16
Ch. 17
Ch. 18
Ch. 19
Interlude D
Unit 5:
Ch. 20
Ch. 21
Ch. 22
Ch. 23
Ch. 24
Ch. 25
Ch. 26
Ch. 27
Ch. 28
Ch. 29
Ch. 30
Interlude E
Unit 6:
Ch. 31
Ch. 32
Interlude F
Unit 7:
Ch. 33
Ch. 34
Ch. 35
Ch. 36
Ch. 37
Ch. 38
Interlude G

» Getting Started » A Guide to the Reading » Tying it all together

Getting Started

Below are a few questions to consider prior to reading Chapter 28. These questions will help guide your exploration and assist you in identifying some of the key concepts presented in this chapter.

  1. What physical and chemical barriers do we possess as a first line of defense against pathogens? 
  2. What is the difference between a nonspecific immune response and a specific immune response to a pathogen?
  3. How is our inflammatory response to a wound coordinated?
  4. What role do white blood cells play in the nonspecific response?
  5. What are the cells involved in the specific immune response?
  6. How does the body acquire immunity from pathogens?
  7. What is an autoimmune disease?

A Guide to the Reading

When exploring the content in Chapter 28 for the first time, the following concepts typically give students the most difficulty. For each concept, one or more references have been identified which may help you gain a better understanding of these potentially problematic areas.

Pathogens and hosts

All organisms are potential hosts for infectious agents or pathogens.  These can include bacteria, protists, viruses, fungi, and multicellular parasites.  Organisms have evolved methods to defend themselves against both internal and external attack by pathogens.  An attack on a host by a parasite has three main steps: finding the host, breaking through the outer body surface, and then harming the host.  An organism’s body wall and the lining of the lungs and gut serve as a first line of defense against attack.  The outermost layer of the skin provides an excellent barrier to pathogens.  The body produces numerous chemicals that act as antibacterial chemicals to destroy bacteria before they have the chance to enter the body.  Pathogens are able to breach this first line of defense and penetrate the body wall through openings in the body wall at wounds.  For this reason, organisms have mechanisms to quickly repair wounds.  If a pathogen gets past the first line of defense of a host, cells within the host recognize specific proteins or carbohydrates on the surface of the pathogen as foreign.  The presence of foreign pathogens initiates the nonspecific and specific immune responses.

For more information on this concept, be sure to focus on:

  • In Section 28.1, Pathogens have ways of crossing the body’s physical barriers
  • In Section 28.2, Detecting pathogens requires distinguishing “self” from “other”
  • Figure 28.2, Getting Past Our First Line of Defense

The Body’s Nonspecific Response

Exposure to an invader triggers a series of rapid nonspecific immune responses within the body. Different types of white blood cells within the body carry out these nonspecific responses to a pathogen.  If we look at a wound on the surface of the body, we see that white blood cells play a large role in countering the wound and any pathogens present.  Macrophages are white blood cells that destroy pathogens that may have entered the body at a wound by engulfing them by phagocytosis.  White blood cells play a role in the inflammatory response to tissue damage as well.  When white blood cells known as mast cells are damaged at the site of a wound, they release histamines, which stimulate the release of prostaglandins.  These prostaglandins in turn dilate blood vessels to increase blood flow to the wound.  Histamines also increase the porosity of capillaries, so that white blood cells can easily leave them, allowing them to attack pathogens outside of the blood stream.  The body also stimulates the clotting of the blood at the site of a wound to trap any pathogens that might be present.  These blood clots are produced by platelets that become sticky and clot. 
            The plasma has about 20 different complement proteins that circulate in the blood and attack invading cells at a wound by poking holes in their plasma membrane.  The complement proteins signal many nutrophil white blood cells to the site of the wound where they attack the pathogens.   This is followed by an increase in the number of macrophages that attack pathogens and then help to clean up dead tissue at the wound.  Natural killer cells are another type of white blood cell that produce holes in pathogen cells or trigger them to commit suicide.  Natural killer cells are summoned to cells infected with viruses by interferons.

For more information on this concept, be sure to focus on:

  • In Section 28.3, The inflammatory response prepares an injured site for defense against pathogens
  • In Section 28.3, White blood cells and defensive proteins mount nonspecific attacks on any pathogens present
  • Figure 28.3, Macrophages Eat Our Microscopic Enemies
  • Figure 28.4, Some Players on the Nonspecific Defense Team

The Human Immune System

The immune system provides the body with immunity from specific pathogens.  The immune system depends on the lymphatic system, which is composed of lymphatic ducts that return white blood cells and proteins from the interstitial fluid back to the cardiovascular system.  Lymph nodes contain white blood cells and act to trap pathogens and foreign particles.  The immune system relies on two types of lymphocytes or white blood cells known as B cells and T cells to help bring about the specific immune response to a pathogen.  As the name lymphocyte suggests, these cells tend to hang out in the lymphatic system.  Antigens are chemical labels on the surface of a pathogen that trigger the B cells to produce specific protein antibodies against those antigens. The antibodies circulate in the body and bind to a pathogen’s antigens and mark it for destruction by macrophages and lymphocytes.  This produces a humoral immunity as the antibodies circulate in the blood and interstitial fluid looking for the specific antigen.  T cells bind with the antigen and produce a cell-mediated immunity.  Helper T cells bind with specific antigens and stimulate the reproduction of B cells and killer T cells.  The killer T cells act by recognizing infected host cells and destroying them.
When we are exposed to a pathogen for the first time, we exhibit a slow primary immune response that involves clonal selection, an increase in the number of B cells and T cells.  Some of these clonal cells become effector cells that fight the pathogen, while others become memory cells that help the body remember the specific pathogen.  The immune system relies on these memory cells that linger from the first exposure to produce a quicker and stronger response to a second exposure to the specific antigens from the pathogen.  This is the basis for the long-lasting immunity conferred by vaccination against specific diseases.

For more information on this concept, be sure to focus on:

  • Section 28.4, Our Third Line of Defense:  The Immune System
  • Figure 28.6, The Human Immune System
  • Figure 28.10, How Antibodies Work
  • Figure 28.11, Helper T Cells
  • Figure 28.12, Killer T Cells Destroy Infected or Damaged Host Cells
  • Figure 28.13, Primary versus Secondary Immune Responses

Tying it all together

Several concepts presented in this chapter build upon concepts presented in previous chapters and are also revisited and discussed in greater detail in subsequent chapters, including:

Immune Response to Disease

  • Interlude B, Applying What We Learned: Cancer: Cell Division Out of Control
  • Chapter 15 – in Section 15.3, Genetic engineering is used to transfer genes from one species to another

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