Campbell Biology Chapter 43 Review: The Immune System

43.1 Innate defenses: barriers, phagocytes and inflammation

pp. 930–935

On the AP exam? Background

Innate immunity isn't required content in the current course, but it runs on tested ideas: receptors binding specific molecules (Topic 4.2), local signals like histamine (Topic 4.1), and engulfing and digesting by endocytosis and lysosomes (Topics 2.5 and 2.1).

In the course: Topic 4.1 Cell Communication, Topic 4.2 Introduction to Signal Transduction, Topic 2.5 Membrane Transport, Topic 2.1 Cell Structure and Function (notes, videos and more questions)

Key points

Every animal, and every plant too, has innate immunity: defenses that are ready from birth, act within minutes to hours, and react the same way however many times a microbe has visited before.
The first line is keeping microbes out. Skin, the mucus-coated linings of the gut and airways, and their secretions block entry. Mucus traps particles, cilia sweep it up and out of the airways, and stomach acid and the enzyme lysozyme in tears and saliva kill many microbes. An insect's chitin exoskeleton does the same job.
Innate receptors spot broad 'signatures' that microbes have and animal cells lack, such as the flagellin protein of bacterial flagella, the lipopolysaccharide on many bacteria, or the double-stranded RNA of some viruses. Toll-like receptors (TLRs) are one important family of these sensors, found in similar forms from flies to people.
Phagocytes (neutrophils, macrophages and dendritic cells) swallow microbes by phagocytosis, a kind of endocytosis. The vesicle then fuses with a lysosome, whose enzymes and toxic chemicals destroy what's inside. Dendritic cells then carry pieces to lymph nodes to start the adaptive response.
Other innate tools: natural killer cells destroy virus-infected or cancerous body cells, often ones that have lost their normal class I MHC markers; interferons warn nearby cells to resist viruses; complement proteins in the blood coat microbes and punch holes in them; and antimicrobial peptides tear microbial membranes.
Inflammation is a local response to injury or infection. Mast cells release histamine and immune cells release cytokines, so nearby capillaries widen and leak, bringing fluid, phagocytes and defense proteins to the spot. That causes the redness, heat, swelling and pain. Fever is a body-wide response.
Some pathogens get past innate defenses, for example with a slippery outer capsule that phagocytes can't grip, or by surviving inside the very phagocytes that swallow them.

Key terms (15)

innate immunity: Defenses an animal is born with. They act within minutes to hours and respond the same way every time a given kind of microbe shows up.
barrier defense: A physical or chemical wall that keeps microbes from getting in at all, like skin, mucus, stomach acid or an insect's exoskeleton.
lysozyme: An enzyme in tears, saliva and mucus that breaks down the cell walls of many bacteria.
Toll-like receptor (TLR): One of a family of receptors on immune cells. Each recognizes a molecule typical of a group of microbes, such as flagellin or viral double-stranded RNA, and switches on innate defenses.
phagocytosis: 'Cell eating.' A cell wraps its membrane around a microbe or particle and pulls it inside a vesicle, which then fuses with a lysosome so the contents get digested.
neutrophil: The most common white blood cell. Neutrophils rush from the blood into infected tissue and engulf microbes.
macrophage: A large phagocyte that lives in tissues and organs. It engulfs microbes and debris and can show pieces of what it ate to T cells.
dendritic cell: A phagocyte in tissues that face the outside world, like skin. After engulfing microbes, it travels to a lymph node and gets the adaptive response started.
natural killer (NK) cell: An innate white blood cell that kills virus-infected or cancerous body cells, especially ones with missing or abnormal surface markers. It doesn't engulf them; it makes them self-destruct.
interferon: A signaling protein released by virus-infected cells. It makes neighboring cells switch on defenses that slow viral reproduction.
complement system: A few dozen blood proteins that switch each other on in a chain. They coat microbes for engulfing, call in immune cells and can punch holes in microbial membranes.
inflammatory response: The local reaction to injury or infection: capillaries widen and leak, so fluid, white blood cells and defense proteins reach the spot. You notice it as redness, heat, swelling and pain.
histamine: A signal released by mast cells that makes nearby blood vessels widen and become leakier. It drives inflammation and allergy symptoms.
cytokine: A small signaling protein that immune cells use to talk to each other, for example to call in more cells or switch other cells on.
lymphatic system: A network of vessels and lymph nodes that collects fluid from tissues, filters it past immune cells and returns it to the blood.

Check yourself: 43.1 Innate defenses: barriers, phagocytes and inflammation

4 questions on 43.1 Innate defenses: barriers, phagocytes and inflammation. Pick an answer to see if you got it, and why.

Question 1 of 4

Which statement correctly describes innate immunity?

Question 2 of 4

Researchers infected normal mice and mice lacking receptor R with one of three bacterial strains and recorded survival after 7 days (invented data). Strain | Has flagella? | Normal mice surviving (%) | Mice lacking R surviving (%) 1 | Yes | 90 | 20 2 | Yes | 85 | 25 3 | No | 88 | 86 Which hypothesis is best supported?

Question 3 of 4

Within an hour of getting a small cut on her finger, a student notices that the area is red, warm and swollen. Which explanation of the swelling is most accurate?

Question 4 of 4

A rare mutation leaves a person's macrophages able to recognize and engulf bacteria normally, but the vesicles holding the engulfed bacteria never fuse with lysosomes. What is the most likely result?

0 of 4 answered

43.2 How B and T cells recognize specific invaders

pp. 935–940

On the AP exam? Background

Receptor diversity, clonal selection and immune memory aren't required in the current course. The tested ideas underneath are protein shape and binding (Topic 1.7), cells recognizing each other by direct contact (Topic 4.1), apoptosis (Topic 4.3), cell division (Topic 4.5) and RNA splicing (Topic 6.3).

In the course: Topic 4.1 Cell Communication, Topic 1.7 Proteins, Topic 4.3 Signal Transduction Pathways, Topic 4.5 Cell Cycle, Topic 6.3 Transcription and RNA Processing (notes, videos and more questions)

Key points

Only vertebrates have adaptive immunity. It's carried out by two kinds of lymphocytes: B cells, which mature in the bone marrow, and T cells, which start there but mature in the thymus. The first response to a microbe is slow, but it's precisely aimed.
An antigen is any molecule a B or T cell responds to, and the small patch that a receptor actually touches is an epitope. One antigen usually has several epitopes. All the receptors on a single lymphocyte are identical, so each cell recognizes one epitope.
A B cell's receptor is a Y-shaped protein made of two heavy and two light chains. The variable regions at the tips of the Y form the binding sites and differ from one B cell to the next; the constant regions are the same. An activated B cell's descendants secrete a free-floating version of this receptor: antibodies.
T cell receptors can't bind free antigens. They recognize only a short fragment of a protein antigen held in an MHC molecule on the surface of a host cell, a display called antigen presentation.
Receptor variety comes from cutting and joining DNA. As each lymphocyte develops, enzymes join one randomly chosen V segment to one J segment (heavy chains also add a D segment) and remove the DNA between them; RNA splicing later links this piece to a constant segment. The change is permanent and copied into every daughter cell, and pairing different chains multiplies the variety.
Young lymphocytes that react to the body's own molecules get mostly destroyed by apoptosis or switched off while they mature, which gives self-tolerance. Regulatory T cells help hold back any that slip through.
When a lymphocyte meets its epitope, that one cell divides into a clone (clonal selection). Short-lived effector cells fight right away, while long-lived memory cells remain, so a second exposure gets a secondary response that is faster, bigger and longer-lasting.

Key terms (15)

adaptive immunity: Defenses found only in vertebrates that recognize specific molecules, take days to build the first time, and remember the invader for next time.
lymphocyte: A type of white blood cell. The lymphocytes of adaptive immunity are B cells and T cells; NK cells are innate lymphocytes.
B cell: A lymphocyte that matures in the bone marrow. When activated, it gives rise to plasma cells that secrete antibodies.
T cell: A lymphocyte that matures in the thymus. Helper T cells coordinate the response, and cytotoxic T cells kill infected cells.
antigen: Any molecule that sets off a response from a lymphocyte, usually a protein or polysaccharide from a microbe.
epitope: The small part of an antigen that a receptor or antibody actually binds. A single antigen can have many different epitopes.
variable region: The tip of each arm of an antibody or receptor. Its amino acid sequence differs between lymphocytes, giving each one its own binding shape.
constant region: The part of an antibody or receptor chain whose sequence is shared by many lymphocytes. It anchors a receptor in the membrane or sets what an antibody does.
antibody: A Y-shaped protein, also called an immunoglobulin, secreted by plasma cells. Each of its two tips binds the same specific epitope.
MHC molecule: A host protein that holds a short peptide in a groove on the cell surface so T cells can inspect it. In humans, MHC proteins are called HLA.
antigen presentation: Displaying a peptide fragment on an MHC molecule at the cell surface, where a T cell with a matching receptor can recognize it.
self-tolerance: The immune system's lack of attack on the body's own molecules, created mostly by removing self-reactive lymphocytes while they mature.
clonal selection: When an antigen binds a lymphocyte's receptor, that one cell is 'chosen' to divide into a clone of identical cells with the same receptor.
memory cell: A long-lived lymphocyte left over from a response. It can launch a fast, strong attack if the same antigen comes back.
secondary immune response: The faster, bigger and longer-lasting response to an antigen the body has met before. Memory cells drive it.

Check yourself: 43.2 How B and T cells recognize specific invaders

4 questions on 43.2 How B and T cells recognize specific invaders. Pick an answer to see if you got it, and why.

Question 1 of 4

Which statement correctly contrasts antigen detection by B cells with antigen detection by T cells?

Question 2 of 4Calculator allowed

In a hypothetical vertebrate, one receptor chain is built by joining 1 of 30 V segments to 1 of 4 J segments. The other chain is built by joining 1 of 50 V segments, 1 of 10 D segments and 1 of 5 J segments. If any version of the first chain can pair with any version of the second, how many different receptors can be made from these segment choices alone?

Question 3 of 4

While maturing in the thymus, a young T cell's receptor binds strongly to a protein found on the body's own cells. What normally happens to this cell, and why does it matter?

Question 4 of 4Calculator allowed

Before infection, about 1 in 100,000 of a mouse's T cells can bind a particular epitope on a virus. Eight days after infection, about 1 in 20 of the T cells in its lymph nodes bind that epitope. By about what factor did the share of matching T cells rise, and what best explains the rise?

0 of 4 answered

43.3 Antibodies, killer T cells and immunization

pp. 940–946

On the AP exam? Yes

Topic 4.1 uses immune cells signaling by direct contact (antigen-presenting cells, helper T cells and killer T cells) as one of its examples of cell communication. You won't be asked to name MHC classes, CD4 or CD8, antibody classes or vaccine types.

In the course: Topic 4.1 Cell Communication, Topic 1.7 Proteins, Topic 5.4 Non-Mendelian Genetics (notes, videos and more questions)

Key points

Adaptive immunity has two arms. In the humoral response, antibodies in blood and lymph deal with microbes and toxins outside cells. In the cell-mediated response, cytotoxic T cells find and kill the body's own cells that are infected.
Helper T cells start both arms. A helper T cell switches on when its receptor meets its matching fragment held by a class II MHC molecule on an antigen-presenting cell (a dendritic cell, a macrophage or a B cell). The two cells stay in direct contact and trade cytokines; then the helper T cell divides and signals cytotoxic T cells and B cells.
Nearly every cell with a nucleus shows fragments of the proteins it makes on class I MHC molecules. In an infected cell, some fragments are viral. A cytotoxic T cell with a matching receptor binds, releases perforin and granzymes, and makes the cell die by apoptosis.
A B cell is activated by its antigen plus signals from a helper T cell. It then forms memory B cells and plasma cells, antibody factories packed with rough ER. As the response goes on, B cells switch antibody class (for example from IgM to IgG) and their antibodies bind more tightly.
Antibodies don't kill microbes by themselves. They neutralize viruses and toxins by covering the parts used to attach to cells, coat microbes so phagocytes grab them (opsonization), clump them together, and trigger complement to punch holes in them.
Active immunity is your own response to an infection or a vaccine, and it leaves memory. Passive immunity is borrowed antibodies, from across the placenta, in breast milk or by injection; it works at once but fades in weeks to months. Vaccines can contain weakened or killed microbes, purified pieces, inactivated toxins, or mRNA that has your cells make one microbial protein.
The same system rejects foreign tissue. Antibodies attack red blood cells of a mismatched ABO type, and foreign MHC molecules on a transplanted organ trigger T cells, so doctors match donors closely and prescribe drugs that suppress the immune response.

Key terms (14)

humoral immune response: The arm of adaptive immunity in which antibodies in blood and lymph deal with microbes and toxins outside cells.
cell-mediated immune response: The arm of adaptive immunity in which cytotoxic T cells find and kill the body's own infected cells.
helper T cell: A T cell that recognizes antigen on class II MHC and then sends cytokine signals that activate cytotoxic T cells and B cells.
cytotoxic T cell: A 'killer' T cell. It recognizes foreign fragments on class I MHC and makes the infected cell die by apoptosis.
antigen-presenting cell: A cell, such as a dendritic cell, a macrophage or a B cell, that takes in antigens and shows pieces of them on class II MHC to helper T cells.
class I MHC: MHC molecules on nearly every cell with a nucleus. They show pieces of proteins made inside the cell, so infected cells can be spotted by cytotoxic T cells.
class II MHC: MHC molecules found mainly on antigen-presenting cells. They show pieces of material the cell has taken in, for helper T cells to check.
plasma cell: The antibody-making form of an activated B cell. It's packed with rough ER for making and secreting protein.
neutralization: Antibodies covering the part of a virus or toxin that it uses to attach to cells, so it can't get in.
opsonization: Coating a microbe with antibodies or complement proteins so phagocytes can grab and engulf it more easily.
active immunity: Protection your own immune system builds after an infection or a vaccine. It includes memory cells and can last for years.
passive immunity: Protection from antibodies made by someone else, received across the placenta, in breast milk or by injection. It works at once but fades in weeks to months.
vaccine: A harmless form or piece of a pathogen, or instructions for making one of its proteins, that trains your immune system and leaves memory cells.
monoclonal antibody: A batch of identical antibodies from one clone of cells, all binding the same epitope. They're used in medical tests and as medicines.

Check yourself: 43.3 Antibodies, killer T cells and immunization

4 questions on 43.3 Antibodies, killer T cells and immunization. Pick an answer to see if you got it, and why.

Question 1 of 4

A helper T cell is activated only after its receptor binds an antigen fragment held by a class II MHC molecule on a dendritic cell, while the two cells stay pressed together and exchange cytokines. Which kind of cell communication does the receptor binding illustrate?

Question 2 of 4

Virus-infected cells lining the airway can be killed by cytotoxic T cells but do not activate helper T cells. Which explanation is most consistent with how T cells recognize antigens?

Question 3 of 4

A virus was mixed with one of three antibody preparations, or with none, and then added to cultured cells. The number of cells that became infected was counted (invented data). Preparation | Cells infected No antibody | 1,000 Antibody to the viral protein that binds host-cell receptors | 30 Antibody to a protein inside the virus's protein coat | 980 Antibody to a bacterial protein | 1,010 Which conclusion is best supported?

Question 4 of 4

A hiker is bitten by a raccoon that may carry rabies, a virus that is almost always fatal once symptoms begin. Doctors inject antibodies against rabies virus around the wound right away and also start a series of rabies vaccine doses. Why give both?

0 of 4 answered

43.4 When immunity misfires or is outsmarted

pp. 946–950

On the AP exam? Background

Allergies, autoimmune diseases and immunodeficiencies aren't required. The tested links are HIV as a retrovirus (Topic 6.4), related viruses swapping genes when they infect the same cell (Topic 6.7), pathogens and drug resistance evolving (Topic 7.8) and cancer as cell division out of control (Topic 4.6).

In the course: Topic 6.4 Translation, Topic 6.7 Mutations, Topic 7.8 Continuing Evolution, Topic 4.6 Regulation of Cell Cycle, Topic 4.1 Cell Communication, Topic 1.7 Proteins (notes, videos and more questions)

Key points

An allergy is an overreaction to a harmless antigen, called an allergen. The first exposure leads plasma cells to make IgE, which sticks to mast cells. On a later exposure, the allergen links neighboring IgE molecules and the mast cells release histamine and other signals. Antihistamines work by blocking histamine's receptors.
Anaphylaxis is the whole-body version: blood vessels widen everywhere, blood pressure crashes and airways tighten within minutes. An injection of epinephrine reverses it.
In an autoimmune disease, self-tolerance breaks down and the immune system attacks the body's own molecules. Examples include type 1 diabetes (T cells destroy the pancreas's insulin-making cells), multiple sclerosis, lupus and rheumatoid arthritis. Risk depends on a mix of inherited genes, surroundings and sex: women develop several of these conditions more often than men do.
Immunodeficiency means a missing or weak response. It can be inborn, as in severe combined immunodeficiency (SCID), where working lymphocytes are nearly absent, or acquired later, from HIV, chemotherapy or drugs given to prevent transplant rejection.
Pathogens evolve ways around immunity. In antigenic variation, a pathogen changes its surface molecules so memory cells no longer match; flu does this by small mutations every year and, now and then, by swapping whole gene segments with flu strains from other animals. In latency, a virus lies quiet inside cells making almost no proteins, as herpesviruses do in nerve cells.
HIV is a retrovirus that enters helper T cells by binding the CD4 protein. Reverse transcriptase copies its RNA into DNA that joins a host chromosome. It mutates quickly, hides in latent cells and kills helper T cells, so untreated infection leads to AIDS and opportunistic infections. Combination drug therapy can keep the virus undetectable for a near-normal lifespan, but it isn't a cure.
The immune system also guards against cancer. T cells and NK cells can recognize abnormal or mutated proteins on cancer cells, and vaccines against cancer-causing viruses like HPV and hepatitis B prevent many cases. Some newer cancer drugs work by releasing the brakes on T cells.

Key terms (13)

allergy: An exaggerated immune response to something harmless, like pollen or pet dander.
allergen: An antigen that triggers an allergy.
IgE: The class of antibody behind most allergies. It sticks to mast cells and makes them release histamine when an allergen binds.
mast cell: A tissue cell full of granules of histamine and other signals, which it releases during inflammation and allergic reactions.
anaphylaxis: A sudden, whole-body allergic reaction in which blood pressure drops and airways narrow. It can kill within minutes and is treated with epinephrine.
autoimmune disease: A disease in which the immune system attacks the body's own molecules or cells, such as type 1 diabetes or multiple sclerosis.
immunodeficiency: A missing or weakened immune response. It can be inborn or acquired later in life.
severe combined immunodeficiency (SCID): An inherited condition in which working B and T cells are nearly absent, so even mild infections can be deadly.
antigenic variation: A pathogen changing the molecules on its surface so that existing antibodies and memory cells no longer recognize it.
latency: A quiet state in which a virus stays inside a host cell, making few or no viral proteins, so the immune system can't detect it.
HIV: Human immunodeficiency virus, a retrovirus that infects and kills helper T cells. Untreated, it causes AIDS.
AIDS: Acquired immunodeficiency syndrome, the late stage of untreated HIV infection, when so many helper T cells are lost that opportunistic infections and certain cancers take hold.
opportunistic infection: An infection by a microbe that rarely sickens people with a healthy immune system but causes serious disease when immunity is weak.

Check yourself: 43.4 When immunity misfires or is outsmarted

4 questions on 43.4 When immunity misfires or is outsmarted. Pick an answer to see if you got it, and why.

Question 1 of 4

A person who is allergic to cat dander had no symptoms the first time he was exposed to it. Which explanation best accounts for this?

Question 2 of 4

A drug that blocks HIV's reverse transcriptase is given to a person living with HIV. Which statement best describes the drug's effect?

Question 3 of 4

The influenza genome is made of eight separate RNA segments. Researchers infect the same cultured cells with two different flu strains at once and find new virus particles carrying some segments from each strain. Why does this finding concern public health experts?

Question 4 of 4

Ten years after recovering from mononucleosis, a healthy adult still carries Epstein-Barr virus DNA in a small number of her memory B cells. She has no symptoms, and her blood contains antibodies against the virus. Which explanation best accounts for how the virus has persisted?

0 of 4 answered