1.        Define the first line of defense mechanisms used to protect the body against pathogens.

Any barrier that blocks invasion at the portal of entry: innate/nonspecific -physical, chemical, genetic barriers

2.        Provide examples of physical, chemical, and genetic barriers. Are they considered a true immune response?

Physical: skin, tears, coughing, sneezing

Chemical: low pH, lysosome, digestive enzymes

Genetic: resistance inherent in genetic makeup of host

3.        Define the second line of defense mechanisms used to protect the body against pathogens and provide examples.

Internalized system of protective cells and fluids which includes inflammation and phagocytosis: innate/nonspecific

-              Inflammatory response, fever, phagocytosis, interferons, complement

4.        Define the third line of defense mechanisms used to protect the body against pathogens and provide examples.

Acquired on an individual basis with exposure to foreign substances; produces protective antibodies and creates memory cells that come into play if the microbe is encountered again: specific

-              Natural or artificial and active or passive

-              T lymphocytes, B lymphocytes, antibodies

5.        What are pathogen-associated molecular patterns? What do they signal? What are pattern recognition receptors?

PAMPs: serve as a red flag to signal WBCs

PRRs: sense pathogens and recognize foreign cells

6.        List the four major subdivisions of the immune system.

Mononuclear phagocyte system (MPS), extracellular fluid (ECF), bloodstream, lymphatic system

7.        What is the mononuclear phagocyte system, and why is it critical to the immune system?

Network of connective tissue fibers that interconnects other cells and meshes with the connective tissue network surrounding organs, allows phagocytic WBCs to move within tissue

8.        Differentiate serum and plasma.

Serum: liquid portion of blood after clot has formed

Plasma: liquid portion of blood with clotting factors

9.        Make a basic diagram to show what myeloid and lymphoid stem cells differentiate into.

10.  Which are the first immune cells to defend against infection? What is their primary function? What do the cytoplasmic granules do?

Neutrophils: phagocytosis

-              Carry digestive enzymes that degrade the phagocytosed material

11.  What do eosinophil granules primarily target? What other conditions will cause the eosinophils to react?

Eukaryotic pathogens, especially larval forms of worm parasites and fungi; also inflammation and allergies

12.   What abnormality would you expect on a WBC in an individual with a helminth infection?

idk

13.  Basophils are the least numerous of all WBCs. What chemical mediators do basophils release? What conditions do they respond to? How do they affect blood vessels?

Release histamine and heparin; inflammation, allergic reactions, asthma; cause blood vessels to dilate in response to injury and helps prevent blood from clotting

14.  What is the difference between basophils and mast cells?

Mast cells are larger and contain more granules than basophiles, have a round nucleus, not bilobar; are nonmotile

15.  Which WBC is the key to the third line or specific immune response? Name the 2 types of cells they differentiate into and where they mature.

Lymphocytes: B cells -bone marrow and T cells -thymus

16.  Which type of lymphocyte provides humoral immunity? How do these cells fight bacterial infections? What is another name for humoral immunity?

B-lymphocytes: secrete antibodies into the bloodstream and lymphatic fluid (antibody-mediated immunity)

17.  Which type of lymphocyte provides cell-mediated immunity? How do these cells fight bacterial infections? What do they become when activated?

T-lymphocytes: attack infected host, cancer, and foreign cells that are marked by the antibodies (helper cells, suppressor cells, cytotoxic)

18.  What do monocytes differentiate into?

Macrophages and dendritic cells

19.  What is the role of a macrophage?

-              process foreign molecules and presents them to lymphocytes

-              specific/nonspecific phagocytic and killing functions

-              secret biologically active compounds that assist, mediate and attract, and inhibit immune cells and reactions

20.  What is the role of the dendritic cell?

-              Trap pathogens

-              Highly effective processors and presenters of foreign proteins

21.  What type of immunity are natural killer (NK) cells involved with?  Why are they not typically considered part of the third line of defense? Does their activation involve immunologic memory?

Innate/nonspecific immunity; because they do not display specificity or involve immunologic memory; NO

22.  What is lymph?

Plasma like-liquid carrier by lymphatic circulation

23.  What is the function of the lymphatic system?

-              Provides an auxiliary route for return of ECF to the circulatory system

-              Acts as a drain-off system for the inflammatory response

-              Rends surveillance, recognition, and protection against foreign material through the use of lymphocytes, phagocytes, and antibodies

24.  Which direction is the movement of lymphatic flow?

One direction: toward the heart; eventually returns to the bloodstream

25.  List the primary and secondary lymphoid organs. When does the thymus start to shrink?

Primary: thymus and bone marrow

Secondary: spleen and lymph nodes

-              Shrinks gradually after puberty

26.  List the actions of the second line of defense and briefly describe each action.

-              Recognition: detect foreign molecules and signal the macrophage to produce chemicals to stimulate an immune response

-              Inflammation: redness, warmth, swelling, pain

-              Phagocytosis: ingest and eliminate materials it finds in tissue compartments ( dead/injured cells, microbes), extract antigens from foreign matter

-              Interferon: bind to cell surface and induce changes in genetic expression, activate the development of WBCs

-              Complement: destroys cells and participates in opsonization

27.   What term describes WBCs migrating out of blood vessels and entering the tissue?

Diapedesis

28.  What circulating substances cause fever?

pyrogens

29.  How is an elevated temperature beneficial for fighting infection?

Inhibits multiplication of temperature-sensitive microorganism, impedes nutrition of bacteria, increases metabolisms and stimulates immune reaction and protective physiological processes

30.  List the phases of phagocytosis and briefly describe each phase.

Chemotaxis: attraction to the inflammatory rxn site by cytokines

Ingestion: engulfment of the cell or particle

Phagolysosome formation: lysosomal adds digestive chemicals and fuses with phagosome

Destruction: lysosomal enzymes destroy microbe

Elimination: debris is released by exocytosis

31.  Complement activates inflammation, destroys cells, and participates in opsonization. What is the end product of the complement system, and how does it affect the cell membrane?

Membrane-attack complex (MAC): produce hundreds of tiny holes in the cell membrane -> cell lyses and death

32.  The third line of defense is an acquired specific immunity. What are the molecules that stimulate this response?

antigens

33.  Describe the two features that characterize acquired immunity.

Specificity: antibodies produced, function only against the antigen that they were produced in response to

Memory: lymphocytes are programmed to recall their first encounter with an antigen and respond rapidly to subsequent encounter

34.  Does cell-mediated immunity involve antibodies? Which T-cells have CD4 receptors? Which T-cells have CD-8 receptors?

No; helper; cytotoxic

35.  Describe where Class I and II MHC genes are located and to which cells they present antigens to.

Class I: found on all nucleated human cells, killer T cells

Class II: found on some types of WBCs, helper T

36.  Define antigen, epitope, immunogens, and haptens.

Antigen: molecule that binds components of the immune response and has the POTENTIAL of invoking an immune response

Epitope: molecular fragment of an antigen that serves as the primary signal to lymphocytes that the molecule is foreign

Immunogens: molecules that ALWAYS provoke a specific immune response when introduced to the body

Haptens: small foreign molecues that are too small by themselves to elicit an immune response

37.  Define alloantigens, superantigens, allergens, and autoantigens.

Alloantigens: cell surface markers and molecules that occur in some members of the same species but not in others

Superantigens: provoke an overwhelming response and massive release of cytokines

Allergens: antigen that evokes allergic reactions

Autoantigens: molecules on self tissues for which tolerance is in inadequate

38.   Define the following antibody-antigen interactions : opsonization, neutralization, agglutination, complement fixation, and precipitation.

Opsonization: process of coating microorganisms or other particles with specific antibodies so they are more readily recognized by phagoctyes

Neutralization: abs fill the surface receptors on a virus or the active site on a microbial enzyme to prevent it from attaching to their target cells

Agglutination: Ab aggregation; cross-linking cells or particles into large clumps renders microbes immobile and increases the speed with which they are phagocytized

Complement fixation: activation of the classical complement pathway can result in the specific rupturing of cells and some viruses

Precipitation: aggregation of free antigen molecules increases the speed they are phagocytized

39.  List the classes of immunoglobulins.

IgG, IgA, IgM, IgD, IgE

40.  Which immunoglobulins can cross the placenta? Which immunoglobulin is involved in allergic and parasitic infections? Which immunoglobulin is the first to be synthesized following an antigen encounter?

IgG, IgE, IgM

41.   What is an anamnestic response, and is it primary or secondary?

Secondary: after second contact with same Ag, immune system produces a more rapid, stronger response due to memory cells

42.  Briefly describe the body’s immune response when T cells are exposed to superantigens.

Drastic consequences: provokes an overwhelming immune response by large numbers of T cells (cytokines, vessel damage, toxic shock, multiorgan damage)

43.  Briefly explain natural, artificial, active, and passive immunity.

Natural: acquired as part of normal life experiences

Artificial: acquired through a medical procedure

Active: results when a person is challenged with antigen that stimulates production of antibodies; creates memory, is lasting

Passive:

44.  Give examples of natural active immunity, natural passive immunity, artificial active immunity, and artificial passive immunity.

Natural: breast milk, developing immunity from measles

Artificial: vaccine, immune serum

Active: fighting off a cold, flu

Passive: antibodies from mother

45.  What is a live attenuated vaccine? Should this type of vaccine be used in immunocompromised individuals? Give examples.

Contain live virus particles or bacterial cells; no; MMR, chickenpox, yellow fever, TB, typhoid (oral)

46.  What is an inactivated vaccine? Give examples. Why do these vaccinations require boosters?

Contain whole bacterial cells or virus particles that have been killed or inactivated; microbe does not multiply; Hep A, Flu, Polio, rabies, typhoid (shot)

47.  What is a viral vector vaccination? Give examples.

Uses a modified version of a different virus to deliver protection; Ebola and COVID

48.  What is a subunit/acellular vaccine?

Vaccine made from bacterial cell parts -acellular (pneumonia, meningitis)

Vaccines made from viruses -subunit (hep B, HPV, shingles)

49.  What is a toxoid vaccine? Give examples.

Consists of a purified fragment of bacterial exotoxin that has been inactivated (diptheria, tetanus)

50.  What is herd immunity?

Resistance to the spread of an infectious disease within a population that is based on pre-existing immunity

51.  Differentiate hypersensitivities, autoimmune diseases, and immunodeficiency diseases.

Hypersensitivities: an exaggerated, misdirected expression of immune responses

Autoimmune: abnormal responses to self Ag due to inability to distinguish between self and nonself

Immunodeficiency: deficiency or loss of immunity

52.  Type I hypersensitivity is an immediate onset of allergies after contact with an allergen. This is an IgE-mediated response. Describe the two levels of severity and give examples.

Atopy: chronic local allergy such as allergic rhinitis, eczema, hay fever, asthma

Anaphylaxis: systemic, often explosive reaction that involves airway obstruction and circulatory collapse

53.  Differentiate the sensitizing dose of an allergen and the provocative dose. Which one precipitates the first signs and symptoms of an allergy?

Sensitizing: first contact with an allergen, primes immune system for subsequent encounter but doesn’t elicit symptoms

Provocative: precipitates the first signs and symptoms that the allergy exists

54.  Mast cells and basophils release chemical mediators. List these chemical mediators and describe the role of histamine.

Histamine, heparin, serotonin, leukotriene, prostaglandins, bradykinin, platelet activating factor

-              Fastest acting and most abundant allergic mediator; potent stimulator of smooth muscle, glands, and eosinophils

55.  Serotonin has been shown to decrease CNS activity. What has it been shown to increase?

Vascular permeability, capillary dilation, smooth muscle contraction, intestinal peristalsis, respiratory rate

56.  Which chemical mediator induces gradual contraction of smooth muscle and is responsible for prolonged bronchospasm, vascular permeability, and mucous secretions in the asthmatic patient?

Leukotrienes

57.  What occurs when prostaglandins are released in response to an allergy?

Vasodilation, increased vascular permeability, increased sensitivity to pain, bronchoconstriction

58.   List the treatment options for Type I hypersensitivity and the goal of treatment. You do not need to list the specific medications.

Avoidance of allergen, desensitization therapy, medications that block the action of lymphocytes, mast cells, or chemical mediators

-              Block progress of allergic response somewhere along the route between IgE production and the appearance of symptoms

59.  Type II hypersensitivities are antibody-mediated and most commonly target what type of cells? What do you mix with a person’s blood sample when blood typing?

RBCs; antiserum that contains anti-A and anti-B -> watch for agglutination

60.  Which blood type is considered the universal donor? Which blood type is considered the universal recipient?

O; AB

61.   Blood transfusions can cause mild reactions like fever, pruritis, and urticaria. Describe what happens in the more acute severe hemolytic transfusion reaction.

-massive hemolysis -> triggers complement and coagulation cascade -> systemic shock and kidney failure; death is common

62.  Rh factor is present in 85% of humans. What is the concern if a mother does not have Rh factor? What is a mother immunized with to prevent this condition?

Hemolytic disease of the newborn; RhoGAM

63.  What is a localized Type III hypersensitivity and a systemic Type III hypersensitivity?

Localized: arthus rxn – local reaction to second inject of Ag at same site as the first, injection site becomes warm, erythematous and tender due to local tissue destruction, usually self limiting

Systemic: serum sickness - results from injection of foreign proteins, condition can become chronic due to the deposition in the organs and cause lymphadenopathy, rashes, arthralgias, fever, renal dysfunction

64.  Why are Type IV hypersensitivities called delayed-type hypersensitivity? Which cells are involved in this process? Provide examples of a delayed allergic response.

Symptoms arise one to several days following a second exposure to an antigen; poison ivy, jewelry, cosmetics; T cells

65.   Differentiate between autograft, isograft, allograft, and xenograft.

Autograft: recipient also serves as donor

Isograft: tissue from identical twin is grafted

Allograft: genetically different individual but of the same species

Xenograft: individuals of different species

66.  Describe what happens to the immune system in autoimmune disease. List some disease symptoms secondary to these deposits.

Immune system loses tolerance to self and forms antibodies and sensitized T-cells against self antigens; SLE, RA, hashimotos, MG, MS DMT1

67.  Where do the autoantibody/autoantigen complexes get deposited?

Basement membranes of multiple organs

68.  Where do the immune complexes bind in individuals with rheumatoid arthritis? What is the result of these complexes activating an inflammatory response?

Synovial membrane of joints; chronic inflammation, development of scar tissue and joint destruction

69.   Differentiate between Grave’s disease and Hashimoto’s thyroiditis.

Graves: autoantibodies cause thyroxin secretion -> hyperthyroidism

Hashimotos: autoantibodies destroy follicle cells -> inactivation of thyroxin -> hypothryoidism

70.  Differentiate between myasthenia gravis and multiple sclerosis.

MG: autoantibodies bind to Ach receptors -> skeletal muscle weakness; inflammation can cause paralysis

MS: damage/lesions to myelin sheath by Tcells and autoantibodies -> paralyzing neuromuscular disease -> muscular weakness, neurological signs, some paralysis

71.  Differentiate between primary and secondary immune diseases. What is the most recognized secondary immunodeficiency disease?

Primary: genetic and present at birth (lack of B or T cell activity)

Secondary: acquired after birth and caused by natural or artificial agents (infection, cancers, chemotherapy, radiation) HIV most recognized

72.  Why does the immune system fail in cancer?

Cancer cells may not be immunogenic enough or cells may retain self-markers and not be targeted