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Temple A&P > Lecture: Resistance and Immunity > Flashcards

Lecture: Resistance and Immunity Flashcards

1
Q

Explain the 3 lines of defense mechanisms.

A

1) first line
- external barriers
2) second line
- phagocytic cells
- antimicrobial proteins
- immune surveillance
- inflammation
- fever
3) third line
- specific immunity

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2
Q

Name 2 examples of external barriers.

A

skin & mucous membranes

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3
Q

Explain the 2 kinds of protection that skin provides.

A

1) mechanical protection
- keratinized cells of the epidermis
- regular shedding of outer layers
2) chemical protection
- sebum from sebaceous glands
- acid mantle (pH 3-5)
- -defensins
- -lactic acid

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4
Q

Define: acid mantle.

A

thin film of lactic and fatty acids on skin that inhibit bacterial growth

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5
Q

Define: defensins.

A

peptides on skin that destroy bacteria, viruses, and fungi

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6
Q

Explain how mucous membranes serve as external barriers to provide nonspecific resistance.

A

mucous traps microbes and foreign substances in body cavities open to the outside: respiratory, digestive, urinary, and reproductive tracts;
fluids (mucus, saliva, tears) contain lysozyme

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7
Q

Define: lysozyme.

A

enzyme present in mucus, saliva, and tears that destroys bacteria by dissolving their cell walls

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8
Q

What lines of defense do phagocytic cells play a role in? Describe the 5 different types of phagocytic cells.

A

2nd & 3rd lines of defense;

1) neutrophils kill bacteria via phagocytosis and respiratory burst
2) eosinophils kill parasites and allergens; produce toxic proteins and anti-histamine
3) basophils secrete histamine (inflammation) and heparin (anticoagulant)
4) lymphocytes, including natural killer (NK) cells
5) monocytes transform into macrophages in tissue

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9
Q

Define: respiratory burst.

A

chemical rxn utilized by neutrophils that forms highly toxic products which form a killing zone around the neutrophil

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10
Q

Explain how antimicrobial proteins serve as a second line of defense.

A 
provide short term resistance against bacteria and viruses;
interferons: 
-prevent multiplication of virus;
-activate NK cells and macrophages;
-may promote cancer cell destruction
complement system
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11
Q

Define: interferons.

A

proteins secreted by infected leukocytes that alert neighboring cells and protect them from becoming infected;
prevent multiplication of virus;
activate NK cells and macrophages;
may promote cancer cell destruction

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12
Q

Define: complement system. What are the 3 pathways?

A

group of globulins that contribute to specific and non-specific immunity;
produced by liver;
always present in blood plasma, activated by pathogens;
3 pathways:
1) classical
2) alternative
3) lectin

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13
Q

Explain the 4 end results of the complement system.

A

1) inflammation: C3a stimulates basophils, neutrophils, and macrophages to secrete histamine and other inflammatory chemicals
2) immune clearance via precipitation: C3b binds Ag-Ab complexes to RBCs; macrophages of liver and spleen remove the complexes
3) phagocytosis: C3b assists phagocytes by means of opsonization
4) cytolysis: C3b combines with other complement proteins to form a membrane attack complex

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14
Q

Define: opsonization.

A

process by which C3b coats microbial cells and serves as binding sites for phagocyte attachment

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15
Q

Define: membrane attack complex.

A

hole formed in an enemy cell by C3b and other complement proteins; renders enemy cell unable to maintain homeostasis

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16
Q

Explain immune surveillance as a second line of defense.

A

natural killer cells destroy:

  • bacteria
  • transplanted cells
  • viruses
  • cancer cells
  • produce perforins and granzymes
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17
Q

Define: perforins.

A

proteins released by NK cells which polymerize in a ring and create a hole in an enemy cell’s plasma membrane

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18
Q

Define: granzymes.

A

protein-degrading enzymes released by NK cells that enter pores made by perforins

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19
Q

Explain inflammation as a second line of defense.

A

local defensive response to tissue injury:
-limits spread and destroys pathogens
-removes damaged tissue
-initiates tissue repair;
cardinal signs: redness, heat, swelling, pain;
suffix = “itis”

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20
Q

What are the 3 stages of inflammation? What are they regulated by?

A

1) mobilization of defenses
2) containment/destruction
3) tissue cleanup and repair;
regulated by cytokines with paracrine/autocrine effects

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21
Q

Define: cytokines.

A

small proteins that serve as a chemical communication network among immune cells

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22
Q

Explain the 3 step process of the mobilization of defenses stage of inflammation.

A

1) local hyperemia: vasoactive chemicals (histamine, kinins, leukotrienes) cause vasodilation
2) margination: ECs produce CAMs called selectins which snag leukocytes
3) diapedesis (emigration): leukocytes enter gaps between ECs and enter tissue fluid of damaged tissues

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23
Q

Define: hyperemia.

A

increased blood flow

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24
Q

Explain the containment/destruction of pathogens stage of inflammation.

A

containment: fibrinogen sequesters enemy cells and heparin prevents clotting in immediate area of injury;
destruction: neutrophils exhibit chemotaxis: attraction to chemicals (bradykinin and leukotrienes) that guide them to site of injury/infection;
neutrophils engage in phagocytosis;
neutrophils secrete cytokines: recruit neutrophils/macrophages and promote leukopoiesis via colony-stimulating factors (CSF)

25
Q

Explain the tissue cleanup and repair stage of inflammation.

A

monocytes turn into macrophages, powerful phagocytes which activate specific immune responses;
edema promotes lymphatic drainage;
dead macrophages/neutrophils pool into a yellowish fluid called pus;
platelet-derived growth factor stimulates fibroblasts to multiply and synthesize collagen

26
Q

Explain how fever serves as a second line of defense.

A 
fever, a.k.a. pyrexia, febrile (febrile = pertaining to fever);
adaptive mechanism:
-promotes interferon activity
-increases metabolic rate
-accelerates tissue repair
-inhibits bacteria/virus reproduction
27
Q

What are the 6 stages of fever?

A

1) Infection and pyrogen secretion:
neutrophils and macrophages secrete Interleukin-1, a polypeptide that acts as an endogenous pyrogen» stimulates anterior pituitary to release Prostaglandin E (raises body temp)
2) hypothalamic thermostat resets to higher set point
3) onset (body temp rises)
4) stadium (body temp oscillates around new set point)
5) infection ends, set point returns to normal
6) defervescence (body temp returns to normal)

28
Q

Define: pyrogen.

A

fever-producing agent

29
Q

What is the function of the immune system in terms of specific immunity?

A

recognizes specific foreign substances and immobilizes, neutralizes, or destroys them

30
Q

What are 2 characteristics of specific immunity?

A

1) specificity: directed against a particular pathogen

2) memory: re-exposure triggers rapid and strong response

31
Q

What are the 2 general forms of immunity?

A

1) cellular (cell-mediated) immunity
- lymphocytes attack and destroy pathogens inside cells
2) humoral (antibody-mediated) immunity
- indirect attack of pathogens in body fluids via antibodies

32
Q

Describe the 4 alternate classifications of immunity.

A

1) natural active: due to natural exposure to antigen (pathogen)
2) artificial active: due to artificial exposure to antigen (pathogen); i.e. vaccination
3) natural passive: antibodies from another person; i.e. mother to fetus
4) artificial passive: injection of an immune serum from person or animal; i.e. snakebites, botulism, tetanus, rabies

33
Q

Define: antigen. What are some examples?

A

any molecule that triggers immune response by being recognized as foreign by the immune system;
ex: free molecules such as toxins and venoms; components of PM or bacterial cell walls

34
Q

Define: epitopes.

A

antigenic determinants;
specific regions of an antigen molecule that stimulate immune responses;
several different epitopes may exist on one antigen, stimulating production of different antibodies and activating T cells

35
Q

Define: haptens.

A

v small molecules that combine with host macromolecules to stimulate immune responses;
responsible for many allergic reactions

36
Q

Explain the basics of immune responses using the terms “antigen” and “antibodies.”

A

after the first encounter with an antigen, the immune system generates antibodies in response for the next encounter;
immune system learns to differentiate between “self-antigens” and “non-self-antigens”

37
Q

What are the 3 classes of lymphocytes? Where are each found?

A

1) Natural Killer (NK) cells
2) T Lymphocytes
- bone marrow
- thymus
3) B lymphocytes
- bone marrow
- lymph nodes
- spleen
- mucuous membranes

38
Q

Explain the 3 stages of the development of T-lymphocytes.

A

1) birth: born in red bone marrow as descendants of PPSCs
2) maturation: T cells respond to hormones in the thymus which stimulate them to develop surface antigen receptors: now they are immunocompetent, and they are given a “final exam”
3) deployment: naive lymphocyte pools colonize lymphatic tissues, “ready for battle”

39
Q

Elaborate upon how maturing T cells are “tested” for sufficient immunocompetence. Discuss selection and deletion.

A

T cells are given a “final exam” during maturation in the thymus;
If they fail, they are eliminated (negative selection). 1 form of negative selection = clonal deletion, in which self-reactive T cells die and macrophages phagocytize them;
If they pass, they multiply and form clones programmed to respond to a particular antigen (positive selection: clonal selection).

40
Q

Explain the development of B-lymphocytes.

A 
process similar to T-lymphocytes;
become immunocompetent in bone marrow;
self-reactive: clonal deletion;
self-tolerant: clonal selection;
abundant in lymph nodes, spleen, bone marrow, and mucous membranes
41
Q

Define: antigen-presenting cell (APC). Name 4 examples.

A 
aid T cells in recognition of antigens;
ex:
B cells
macrophages
reticular cells
dendritic cells
42
Q

Explain the major histocompatability complex (MHC).

A

proteins on APC surface;
“holds” foreign antigen and processes it;
initiates attack on non-self antigens via T cells

43
Q

What are 4 different types of T lymphocytes that play a role in cellular immunity?

A

1) cytotoxic T cells
- killer
2) helper T cells/
- promote cytotoxic T cells and humoral immunity
3) memory T cells
4) suppressor T cells
- regulate response

44
Q

What are the 3 stages of cellular immunity?

A

1) recognize: antigen presentation followed by T cell activation
2) react: helper T cells aid in immune response while cytotoxic t cells directly attack/kill invaders
3) remember: T cell recall response

45
Q

Explain the 2 key events that occur during the recognition phase of the cellular immune response.

A

1) antigen presentation: APC migrates to lymph node and presents to T cells:
MHC-I proteins are present in every cell except RBCs;
cytotoxic cells respond;
MHC-II proteins occur only on APCs and display only foreign antigens;
helper T cells respond
2) T cell activation:
successful costimulation (“double-checking” of APC) activates process of clonal selection: effector cells and memory T cells

46
Q

Explain the role of helper T cells and cytotoxic T cells in the attack phase of the cellular immune response.

A

helper T cells secrete interleukins which have 3 effects:

1) attract neutrophils and NK cells
2) attract macrophages
3) stimulate T and B cells;

cytotoxic T cells deliver a "lethal hit" of cytotoxic chemicals:
perforin
granzymes
interferons
tumor necrosis factor (TNF)
47
Q

Explain the “remember” phase of the cellular immune response.

A

recruitment by helper T cells causes initial immune response against pathogen;
primary response peaks in ~1 week;
next time, memory cells made during clonal selection activate T cell recall response:
-quick attack when pathogens appear
-no noticeable illness: “immunity”

48
Q

What are the 3 stages of humoral immunity?

A

1) recognition
- antigen recognition
- antigen presentation
- clonal selection
- differentiation
2) attack
- neutralization
- complement fixation
- agglutination
- precipitation
3) memory

49
Q

What are the 4 phases of the recognition stage of the humoral immune response?

A

1) antigen recognition: immmunocompetent B cell is exposed to antigen
2) antigen presentation: B cell internalizes antigen and displays processed epitope. Helper T cell binds to B cell and secretes interleukin.
3) clonal selection: interleukin stimulates B cell to divide repeatedly and form a clone.
4) differentiation: some cells of the clone become memory B cells. Most differentiate into plasma cells.

50
Q

Describe antibodies. Where are they found? What is their structure?

A 
a.k.a. immunoglobulins (Igs) = gamma globulins found in blood plasma, body secretions, and leukocyte membranes;
basic structural unit = antibody monomer, composed of 2 heavy chains and 2 light chains of amino acids;
variable region = unique antigen binding site;
constant region determines antibody class and complement protein binding action
51
Q

Name the 5 antibody classes.

A

1) Immunoglobulin alpha (IgA)
2) Immunoglobulin delta (IgD)
3) Immunoglobulin epsilon (IgE)
4) Immunoglobulin gamma (IgG)
5) Immunoglobulin mu (IgM)

52
Q

What is the role of immunoglobulin alpha (IgA)?

A

blood plasma, mucous, tears, saliva, intestinal secretions;

function: protects epithelium and provides passive immunity to newborn

53
Q

What is the role of immunoglobulin delta (IgD)?

A

acts as a receptor for B cells;

activation of B cells by antigens

54
Q

What is the role of immunoglobulin epsilon (IgE)?

A

transmembrane protein of basophils and mast cells;
stimulates release of histamine (inflammation & allergic rxns);
attracts eosinophils to sites of parasitic infection

55
Q

What is the role of immunoglobulin gamma (IgG)

A

most abundant antibody;
predominant antibody of secondary immune response;
complement fixation;
includes Anti-D antibodies of the Rh blood group;
crosses placenta to newborn for temporary immunity

56
Q

What is the role of immunoglobulin mu (IgM)?

A

blood plasma and lymph;
predominant antibody of primary immune response;
complement fixation;
includes Anti-A and Anti-B aggluntinins

57
Q

Explain the attack phase of the humoral immune response. Describe the four mechanisms antibodies use to render antigens harmless.

A

antibodies are released by plasma cells but cannot directly destroy antigens;

1) neutralization: antibody binds to foreign antigen and “covers up” parts that are pathogenic
2) complement fixation: IgM and IgG bind to enemy cells, change shape, and expose complement-binding sites
3) agglutination: antibody binds to multiple antigens, sticks them together, and immobilizes them
4) precipitation: antibody links multiple antigen molecules together, creating a large complex that gets eliminated

58
Q

Explain the memory phase of the humoral immune response.

A

primary response

  • first exposure to antigen
  • appearance of antibodies delayed for ~3-6 days while naive B cells multiply and differentiate into plasma cells
59
Q

Define: antibody titer.

A

level of antibodies in the blood plasma

Temple A&P (15 decks)

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