Review questions – chapter 26
1.All organisms need to defend themselves against infection. Discuss, with examples, how the immune response has evolved over time towards ever-increasing complexity. How has the function of some important molecules changed? (p. 605)
While we know most about human immunology, all organisms are subject to infection and it is reasonable to assume that all have defence mechanisms, even the most primitive. Some of those that are important to a particular branch of the evolutionary tree have been lost in vertebrates, but conversely many have been retained or have evolved further.Of innate defences or acquired immunity, it is the innate defences that are the more ancient. These non-specific defences include physical and chemical barriers to invasion found in most animals and plants, and innate immunity, which refers to cellular non-specific defences that are part of the immune system. Non-specific defences evolved and were added to through evolutionary history, culminating in the highly complex immune system found in humans and higher vertebrates. It was in vertebrates that the capacity for gene rearrangement, which is required to generate a diverse and specific immune response, arose. Thus, primitive animals and plants show only non-specific innate immunity, whereas vertebrates express both innate and specific immunity working together in sophisticated ways.
2.What are the fundamental differences between innate and acquired immunity? Explain the role of each in defence against a viral infection? (pp. 607–612)
The table below summarises the essential differences. All these measures offer some defence against a viral infection.
Innate defence mechanism / Acquired immunityInitial barrier to infection /
Specific for invading pathogen /
Takes time to develop /
Characterised by immunological memory
While non-specific itself, can control induction of the specific response /
Includes:
Low pH in stomach /
Antibodies /
Mucus and cilia to trap microorganisms /
Lymphocytes /
Enzymes in tears /
3.In what ways does the T-cell receptor resemble an antibody molecule and in what ways does it differ? (p. 620)
This question is answered clearly in Table 26.2.
4. Macfarlane Burnet framed three fundamental questions about how the immune response worked. (1) How is the immune system able to recognise such a wide variety of antigens, some of them synthetic chemicals never before encountered and for which a response held no evolutionary advantage?(2) What accounts for immunological memory?(3) Why does the immune system not normally attack the body’s own (self) antigens?
How does clonal selection answer these questions? (pp. 630–631)
This question is the topic of Box 26.4.
5.What is immune tolerance? What happens if it fails? (p. 622)
Immune tolerance is the inability to respond to certain antigens. It is acquired early in embryonic life and is important as it means the body does not respond to self-antigens.
When the body loses tolerance for its own antigens and attacks them, autoimmune disease results. Autoimmune disease results in cellular damage of the body by its own immune system; it is treated with immunosuppressive drugs.
6.Explain how immunological memory works. Why, in rare cases, does immunological memory to one organism provide cross-protection against another? (pp. 610–611)
B cells manufacture antibodies that are expressed on their surface and function as receptors. Some of the B cells will become long-lived memory cells, able to respond to the same antigens years later. When these memory B cells detect the particular antigens for which they have been programmed, they initiate a rapid secondary response to that same antigen. The secondary response has a shorter lag phase, a more rapid log phase and persists for a longer plateau period.
7.Why and how do lymphocytes circulate around the body? (pp. 606–607, 624)
Lymphocytes circulate around the body via the cardiovascular system and the lymphatic system. Specific organs of the lymphatic system are essential to the body’s immune system. The lymphatic organs contain numerous lymphocytes.
Undifferentiated lymphocytes are derived from bone marrow stem cells. Some of these migrate through the blood or lymphatic circulatory system to the secondary lymphoid tissue such as the thymus, spleen or lymph nodes. Those lymphocytes, which migrate to the thymus, undergo processing to become T cells. Some T cells enter the blood stream; others reside in organs of the lymphatic system like the lymph nodes or spleen.
B cells are also derived from undifferentiated lymphocytes. They differentiate in the bone marrow. These B cells are then distributed by the blood and circulate in the body. They also may settle in various lymphoid organs.
Lymphocytes circulate throughout the lymph system within fluid that has seeped out between cells and from the capillary network. The lymph nodes filter out foreign material. This is important when an infection has occurred, as the lymph passes through the nodes the bacteria are removed. Swollen lymph nodes are usually a sign of infection. Thus the lymphocytes circulate the blood and lymph, providing immune surveillance and destruction of pathogens.
8.Explain how the process of gene rearrangement occurs in T and B-lymphocytes to give rise to a wide range of different T-cell receptor (TCR) and antibody molecules. How does this help us to cope with the huge number of antigens in our environment? (p. 620)
A unique property of both antibody molecules and receptors on the T cell (TCR) is their incredible diversity. For example, a human can synthesise more than ten kinds of antibody. This diversity is created by rearrangements of gene segments coding for the antibody molecule (immunoglobulin) and T-cell receptor.
For immunoglobulins (Igs), diversity is the result of shuffling the parts of split or interrupted genes with many exons and splicing together the parts to produce an enormous variety of Ig molecules. If a single B cell binds with a particular antigen, it undergoes clonal expansion to produce many plasma cells producing large amounts of that specifically required antibody.
The T-cell receptors on the plasma membrane surface of T cells are closely related to immunoglobulins in function but they cannot bind antigen free in solution. T cells respond to antigens exposed on the surfaces of antigens presenting cells such as macrophages. The macrophages present the antigen fragment on their surface as apart of a complex with the histocompatibility antigens. The T cell is triggered when the variable region of its receptor reacts with the antigen on the presenting cell surface. The potential diversity of the TCR comes from the genetic diversity of the variable portion of the antigen-binding site. Due to gene rearrangements, 1015 TCR molecules are theoretically possible.
How does this help us to cope with the huge number of antigens in our environment? It is the gene rearrangements’ coding for the variable region of the TCR and the immunoglobulin molecules that account for the ability of the immune system to respond to a huge number of antigens in the environment.
9.How do T cells regulate other cells during immune responses? Draw a diagram showing the cell interactions involved in generating an antibody response. (p. 620)
The interactions of cells and antibodies in the regulation of the immune response are complex.
Antigen (Ag) is presented to T-helper (TH) cells and B cells by an antigen-presenting cell (APC) such as a dendritic cell or macrophage to stimulate them. The TH cells, once activated, help the specific B cells to produce antibody.
10.What is major histocompatability complex (MHC) restriction? Draw a diagram of the interaction of the T-cell receptor with an antigen epitope being presented by an antigen-presenting cell. (pp. 621–622)
Refer to Figure 26.17 and to Table 26.3.