Chapter 22 – Immune System Review

80 Question-and-Answer flashcards covering key concepts from Chapter 22 on the immune system, suitable for exam review.

1. What are the four primary functions of the immune system?

Recognize pathogens, neutralize or destroy them, clear dead or damaged cells, and establish immunologic memory.

2. How do the lymphatic and immune systems cooperate to protect the body?

Lymphatic vessels return interstitial fluid to the blood and filter it through lymph nodes where immune cells survey antigens; lymphoid organs (nodes, spleen, tonsils, MALT) house and activate lymphocytes that carry out immune responses.

3. Define an infectious agent.

Any organism or particle that can cause disease when it invades and multiplies inside a host.

4. What makes an agent "pathogenic"?

Its ability to evade defenses and cause harm, producing signs or symptoms of disease.

5. Name the five major classes of pathogens and give one example of each.

Viruses (influenza virus), bacteria (Staphylococcus aureus), fungi (Candida albicans), protozoa (Plasmodium species), multicellular parasites (tapeworms).

6. What is a cytokine?

A small, soluble protein released by immune or other cells that acts as a chemical messenger to coordinate immunity, inflammation, or hematopoiesis.

7. Give two key differences between innate and adaptive immunity.

Innate is fast and nonspecific with no memory; adaptive is slower to start, highly specific, and generates memory for future protection.

8. List three hallmark characteristics of innate immunity.

Present at birth, responds rapidly (minutes–hours), and uses the same defenses against all microbes (nonspecific).

9. What constitutes the first line of innate defense?

External physical, chemical, and biological barriers such as skin, mucous membranes, secretions, and normal flora.

10. What constitutes the second line of innate defense?

Internal nonspecific defenses including phagocytes, NK cells, inflammation, fever, and antimicrobial proteins (interferons, complement).

11. What is the main goal of the first line of defense?

Prevent pathogens from entering body tissues in the first place.

12. What is the main goal of the second line of defense?

Detect and eliminate pathogens that breach surface barriers before they can spread.

13. Give two physical barriers that block pathogen entry.

Intact epidermis of skin and the cilia-lined mucosa of the respiratory tract.

14. Name two chemical barriers that block pathogen entry.

Low pH of gastric juice and the lysozyme enzyme in tears and saliva.

15. What is an example of a biological barrier to infection?

The normal bacterial flora that out-compete potential pathogens on skin or in the gut.

16. What is the primary role of neutrophils in immunity?

They rapidly phagocytose and destroy bacteria and fungi; they are the first leukocytes to arrive at most infections.

17. How do macrophages protect the body?

They engulf and digest microbes and debris, release cytokines, and present antigen to T cells to initiate adaptive responses.

18. What dual role do dendritic cells play in immunity?

They are potent phagocytes and the most effective antigen-presenting cells for activating naïve T lymphocytes.

19. What do basophils and mast cells release and what is the effect?

Histamine, heparin, and other chemicals that promote vasodilation and increased permeability, intensifying inflammation.

20. How do eosinophils combat parasites?

They release cytotoxic enzymes and reactive oxygen species onto the surface of multicellular parasites and modulate allergic responses.

21. How do natural killer (NK) cells destroy infected or cancerous cells?

They bind abnormal cells, release perforin and granzymes, triggering apoptosis without prior sensitization.

22. Name the two major antimicrobial protein systems.

Interferons and the complement system.

23. Against what pathogen are interferons especially effective?

Viruses.

24. Briefly explain how interferons defend neighboring cells.

Virus-infected cells secrete interferons that bind to nearby cells, inducing them to produce antiviral proteins that inhibit viral replication.

25. What is the complement system?

A group of ~30 plasma proteins that, once activated, enhance innate and adaptive immunity by a cascade of reactions.

26. Against which type of pathogen is complement most effective?

Extracellular bacteria (especially Gram-negative) and some fungi.

27. List the three chief antimicrobial actions of complement.

Opsonization (C3b coating), cytolysis via membrane-attack complex, and enhancement of inflammation through anaphylatoxins (C3a, C5a).

28. Define inflammation.

A localized, nonspecific defensive response of vascularized tissue to injury or infection.

29. Outline the basic steps of the inflammatory response.

Release of inflammatory chemicals, vasodilation and increased permeability, recruitment of leukocytes (chemotaxis), phagocytosis, and repair.

30. Give two benefits of inflammation.

Isolates and eliminates pathogens and sets the stage for tissue repair.

31. List the four cardinal signs of inflammation.

Redness, heat, swelling, pain (and sometimes loss of function).

32. Define fever (pyrexia).

An abnormally elevated body temperature (≥38 °C or 100.4 °F) caused by a systemic inflammatory response.

33. What is a pyrogen?

Any substance (exogenous or endogenous) that triggers the hypothalamus to raise the set-point for body temperature.

34. Give two advantages of a moderate fever.

Slows microbial reproduction and speeds up tissue repair by enhancing immune cell activity and enzyme function.

35. Name one danger of a very high fever.

Protein denaturation leading to seizures, brain damage, or death.

36. List three properties that distinguish adaptive immunity.

Specificity for particular antigens, systemic (body-wide) protection, and immunologic memory.

37. Differentiate between humoral and cell-mediated immunity.

Humoral immunity is B-cell/antibody-driven and targets extracellular pathogens; cell-mediated immunity is T-cell-driven and targets infected or abnormal cells.

38. Define antigen.

A substance that can be recognized by adaptive immune receptors and provoke an immune response.

39. Distinguish between foreign antigens and self-antigens.

Foreign antigens originate outside the body and are immunogenic; self-antigens are normally tolerated molecules produced by one’s own cells.

40. Define immunogenicity, and explain how a hapten differs from a complete antigen.

Immunogenicity is the ability to provoke an adaptive response; a hapten is a small reactive molecule that becomes immunogenic only when attached to a larger carrier.

41. Differentiate between active and passive immunity.

Active immunity results when the body produces its own antibodies or T cells; passive immunity is gained by receiving ready-made antibodies (no memory formed).

42. What receptor does a T lymphocyte use to recognize antigen?

The T-cell receptor (TCR) bound to CD4 or CD8 coreceptors interacting with MHC-bound antigen.

43. What receptor does a B lymphocyte use to recognize antigen?

Membrane-bound immunoglobulin (B-cell receptor, BCR).

44. State the two major subtypes of lymphocytes.

T lymphocytes and B lymphocytes.

45. Identify the three professional antigen-presenting cells.

Dendritic cells, macrophages, and B cells.

46. How does an APC activate a T cell?

By displaying processed antigen on MHC molecules, providing costimulatory signals, and releasing cytokines.

47. Compare MHC class I and MHC class II molecules.

MHC I are on all nucleated cells and present endogenous peptides to CD8 T cells; MHC II are on APCs and present exogenous peptides to CD4 T cells.

48. Why must donor and recipient HLAs be matched for an organ transplant?

Closer matches reduce the likelihood that recipient T cells will recognize the graft as foreign and attack it.

49. Why are immunosuppressive drugs given after transplantation, and what are two major drawbacks?

They dampen the recipient’s immune response to prevent rejection; drawbacks include higher risk of infection and increased incidence of cancer or drug toxicity.

50. What is a vaccine and how does herd immunity work?

A vaccine is a preparation of antigen that induces active immunity and memory without disease; widespread vaccination protects even unvaccinated individuals by reducing pathogen transmission (herd immunity).

51. Which immune cells are primarily responsible for graft rejection?

Cytotoxic T lymphocytes (with help from helper T cells and NK cells).

52. Summarize the general function of an antigen-presenting cell.

To capture, process, and display antigen fragments with MHC molecules for recognition by T lymphocytes, launching adaptive immunity.

53. Name the three major events in the life of every lymphocyte.

Formation and maturation, activation and clonal selection, and the effector response at infection sites.

54. Where are all lymphocytes initially produced?

Red bone marrow.

55. Where do B cells mature? Where do T cells mature?

B cells in red bone marrow; T cells in the thymus.

56. Why is maturation necessary for lymphocytes?

To equip them with functional antigen receptors and eliminate cells that react strongly to self-antigens.

57. Define immunocompetence.

The ability of a lymphocyte to recognize (via its receptor) one specific antigen and respond to it.

58. Define self-tolerance.

Unresponsiveness of lymphocytes to the body’s own antigens, preventing autoimmunity.

59. What is positive selection of T cells?

Testing whether a T cell’s receptor can bind self-MHC molecules; cells that fail die by apoptosis.

60. What is negative selection of T cells?

Elimination of T cells that bind strongly to self-antigen–MHC complexes, ensuring self-tolerance.

61. What happens to T cells that fail either selection test?

They undergo apoptosis and are removed (clonal deletion).

62. After maturation, where do naïve lymphocytes reside?

Secondary lymphatic structures such as lymph nodes, spleen, and MALT awaiting antigen encounter.

63. In immunology, what does the term “naïve” lymphocyte mean?

A mature lymphocyte that has not yet encountered its specific antigen.

64. What two signals are required for full activation of a lymphocyte?

Antigen recognition through the receptor and a costimulatory signal (often a second receptor–ligand or cytokine).

65. Into what two main populations do activated B cells differentiate?

Antibody-secreting plasma cells and memory B cells.

66. Into what two main populations do activated T cells differentiate?

Effector T cells (helper or cytotoxic) and memory T cells.

67. Define immunodeficiency and distinguish between congenital and acquired forms; how does SCIDS fit this definition?

Immunodeficiency is impaired immune function; congenital is inherited (e.g., SCIDS—lack of B and T cells), acquired develops later (e.g., AIDS). SCIDS leaves victims defenseless without stem-cell therapy.

68. How do helper T cells and regulatory T cells influence immune activity at an infection site?

Helper T cells release cytokines that activate B cells, cytotoxic T cells, and innate cells; regulatory T cells dampen immune reactions, preventing excessive or autoimmune responses.

69. How do cytotoxic T cells eliminate infected cells?

They bind MHC I–antigen complexes and release perforin and granzymes that induce apoptosis in the target cell.

70. What is the chief function of plasma cells?

Produce and secrete large quantities of specific antibodies into body fluids.

71. Why are memory cells critical for long-term immunity?

They persist after infection and mount faster, stronger responses upon re-exposure to the same antigen.

72. Which lymphocyte population is targeted by HIV, and why does this cripple the immune system?

CD4⁺ helper T cells; their loss impairs activation of cytotoxic T cells, B cells, and innate cells, leading to severe immunodeficiency.

73. List the five classes of immunoglobulins.

IgG, IgA, IgM, IgD, IgE.

74. Which immunoglobulin is most abundant in plasma and can cross the placenta?

IgG.

75. Which immunoglobulin is found mainly in mucus and secretions?

IgA, especially as a dimer in saliva, tears, and breast milk.

76. When is IgM produced and what unique structure does it form?

First antibody released in a primary response; forms a pentamer that is excellent at agglutination and complement activation.

77. With which reactions is IgE associated?

Allergic (acute Type I hypersensitivity) reactions and defense against parasitic worms.

78. Describe three major defensive actions performed by antibodies.

Neutralization of toxins/viruses, opsonization to enhance phagocytosis, and agglutination/precipitation of antigens; they also activate complement and facilitate ADCC.

79. What is an acute (Type I) hypersensitivity reaction?

A rapid IgE-mediated reaction to a previously encountered allergen causing mast-cell degranulation, histamine release, and symptoms such as hives or anaphylaxis.

80. What is the difference between a primary and a secondary immune response?

The primary response is slower and produces lower antibody levels upon first antigen exposure; the secondary response is faster and stronger due to memory cells generated in the primary response.