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Immunology > Immunology Exam 1 > Flashcards

Immunology Exam 1 Flashcards

1
Q

Describe the basic functions of the immune system

A
  1. protects the body from pathogens
  2. helps repair damage from physical injury
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2
Q

list the levels of defense against pathogens

A
  1. physical/anatomic barriers (e.g. skin, oral mucosa, respiratory epithelium, and intestine)
  2. complement/antimicrobial proteins (C3, defensins)
  3. innate immunity (macrophages, granulocytes, NK cells)
  4. adaptive immunity (B cells/antibodies, T cells)
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3
Q

differentiate commensal and pathogenic organisms

A

commensal: relationship between host and microbe that is mutually beneficial (e.g. microbiome required for development, nutrition, immune regulation & protects against pathogens)

pathogenic: an organism that causes sufficient damage to result in disease (e.g. virus, bacteria, prions, fungi, protozoa, other parasites)

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4
Q

identify the barrier tissues

A
  1. skin
  2. gut
  3. lungs
  4. eye/nose/oral cavity
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5
Q

identify the protective characteristics of the skin

A

Mechanical: tight junctions & longitudinal flow of air/fluid
Chemical: fatty acids, B defensins, lamellar bodies, cathelicidin
Microbiological: microbiota

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6
Q

identify the protective characteristics of the gut

A

Mechanical: tight junctions & longitudinal flow of air/fluid
Chemical: low pH & enzymes & alpha defensins
Microbiological: microbiota

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7
Q

identify the protective characteristics of the lungs

A

mechanical: tight junctions & movement of mucus by cilia
chemical: surfactant & alpha defensins
microbiological: microbiota

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8
Q

identify the protective characteristics of the eyes/nose/oral cavity

A

mechanical: tight junctions, tears, nasal cilia
chemical: enzymes in tears & saliva & histatins/beta defensins
microbiological: microbiota

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9
Q

compare innate vs adaptive immunity in regard to specificity, action time, persistence, memory, antigens, receptors, examples

A

innate: non specific, immediate, short-lived, no memory, conserved MAMPs, germ-line encoded, neutrophils/macrophages/antigen presenting cells

adaptive: specific, delayed, long-lived, memory, diverse proteins/peptides/carbs, gene segments rearrange to create diversity, T cells/B cells

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10
Q

describe the phases of the immune response

A
  1. innate response (inflammation, complement, phagocytosis, destruction of pathogens) - minutes
  2. adaptive response (B cells, T cells, lymphocytes) - hours/days/weeks
  3. immunological memory (maintenance of memory B cells and T cells and high serum or mucosal antibody levels; protect against reinfection) - days/weeks/lifelong
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11
Q

understand how antibodies and T cells responses lead to a clearance of microorganisms and toxins

A

B cells/Antibodies: neutralization, opsonization/phagocytosis, antibody-dependent cellular toxicity, and complement activation which leads to lysis, phagocytosis with fragment C3b, and inflammation

T cells: cytotoxicity, intracellular immunity (type 1), mucosal and barrier immunity (type 2), and extracellular immunity (type 3)

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12
Q

compare the effector mechanisms of the innate and adaptive immune systems

A

innate
1. cellular (mast cells, neutrophils, eosinophils, basophils, macrophages, innate lymphoid cells)
2. soluble (complement, kinins, vasoactive amines, eicosanoids, defensins, ROS, lysosomal enzymes, cytokines, chemokines, acute phase proteins)

adaptive
1. antibody-mediated immunity: antibodies in the blood (e.g. colostrum)
2. cell-mediated immunity: e.g. rejection of foreign organ graft

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13
Q

what is neutralization, opsonization, and phagocytosis?

A

neutralization: neutralizing antibody coats the pathogen removing its effect

opsonization: coating the pathogen to make it more susceptible to phagocytosis

phagocytosis: when a phagocyte engulfs the pathogen and eliminates it

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14
Q

describe the function of primary and secondary lymphoid organs and where they are located

A

primary/central lymphoid organs: production of vertebrate immune cells, bone marrow/thymus

secondary/peripheral lymphoid organs: maintain naive lymphocytes, initiate an adaptive immune response, lymph nodes/spleen/mucosal lymphoid tissue

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15
Q

what is cell signaling?
understand the basic concepts of cell signaling

A

cell signaling leads to the production of signals that serve as inputs for other cells…

  1. exogenous stimulus (e.g. pathogen) binds to a receptor on the source cell
  2. source cell sends the signal to target cells
  3. target cell generates a response
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16
Q

list the cellular and subcellular location and ligands for key PRR and their microbial/danger ligands

A

TLR 4: membrane-bound, a ligand is LPS, and danger ligand is DAMPS

TLR3,7,8,9: w/in vesicles, dsRNA/ssRNA/CpG DNA which are viruses/bacteria, danger ligand is foreign nucleic acids

complement: soluble

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17
Q

describe the steps involved in innate recognition of pathogens

A
  1. pathogen admit the PAMPs
  2. PRR recognizes/senses the PAMPs
  3. signal transmitted into the nucleus where gene transcription will occur
  4. gene transcription triggers an antimicrobial immune response (inflammatory cytokines, chemokines, type I interferons)
    *endosomal receptors good at triggering type I interferons
    *membrane-bound receptors (TLR4) good at triggering proinflammatory cytokines
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18
Q

where is the origin of vertebrate immune cells? what type of cell do all the cells originate from?

A

origin: bone marrow
all cells originate from pluripotent hematopoietic stem cells (HSCs)

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19
Q

define phagocyte, antigen-presenting cell, Fc receptor

A

phagocyte: cell type capable of ingesting small particles (e.g. neutrophils, macrophages, dendritic cells)

antigen-presenting cell: cells that process and display antigen in the context of MHC to initiate an adaptive immune response (e.g. macrophages, dendritic cells, B cells)

Fc receptor: receptors on the surface of cells that bind the constant region of the antibody molecules

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20
Q

understand the monocyte/macrophage immune surveillance network; describe macrophage activation

A

-monocytes patrol the blood and sense for infection or damage
-monocytes leave the blood and become macrophages which are located in the tissues
-macrophage activation is rapid, reversible, and remarkably plastic

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21
Q

describe the role of mast cells and the initiation of inflammation
- where are they located
- what do they release
- how are they secreted & regulated
- what do they synthesize
- what type of reaction and receptor
- what do they regulate

A

-long-lived residents of vascularized tissues beneath the epithelial surface exposed to the external environment (skin, respiratory, GI tract) around vessels and close to peripheral nerves
-degranulate to release histamine & serotonin (vasoactive amines)
- not killed by degranulation
- secretion is orderly/coordinated
- regulated by endothelium cells
-synthesize prostaglandins and leukotrienes to attract macrophages and PMNC (neutrophils, basophils, eosinophils)
- receptors include Fc (bind IgE) & PRR
- type I hypersensitivity reactions (IgE receptors for allergies)
- regulate eosinophils

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22
Q

describe the lifecycle of a macrophage from birth in the bone marrow to specialized tissue macrophage

A
  1. hemapoitetic stem cell (HSC)
  2. common myeloid progenitor cells (HPC)
  3. granulocyte/macrophage progenitor
  4. monocyte
  5. macrophage type dependent on tissue (e.g. osteoclast, kupffer, histiocyte, white pulp/red pulp)
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23
Q

key characteristics of hematopoietic stem cells and hematopoietic progenitor cells

A

HSC: self renew, proliferate, and differentiate into HPC

HPC (common lymphoid progenitor, common myeloid progenitor, granulocyte/macrophage progenitor, and megakaryocyte/erythrocyte progenitor): do not self renew, proliferate, and differentiate into varied colony forming units that include B cells/T cells/ dendritic cells/ NK cells/ granulocytes/monocytes/platelets/RBC

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24
Q

where do T cells mature?

A

Thymus

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25
Q

where do B cells mature

A

bone marrow first then the spleen

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26
Q

what MHC is specific to WBCs

A

MHC II

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27
Q

what are the differences between macrophages and resident macrophages?

A

resident macrophages: from erythroid myeloid progenitor (EMP), clear cellular debris, iron processing, immune surveillance, response to infection, resolution of inflammation; reside in the tissues; recruit neutrophils

macrophage: from common myeloid progenitor (CMP), come from monocytes in the blood –> tissues, type dependent on tissue

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28
Q

resident macrophages in the liver are called _____

A

Kupffer cells

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29
Q

resident macrophages in the spleen are called _____

A

red pulp macrophages
white pulp macrophages
marginal zone macrophages
metallophilic macrophages

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30
Q

resident macrophages in the lung are called _____

A

alveolar macrophage

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31
Q

resident macrophages in the bone are called _____

A

osteoclast

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32
Q

resident macrophages in the CNS are called _____

A

microglial cells

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33
Q

resident macrophages in the connective tissue are called _____

A

histiocyte

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34
Q

how do mast cells regulate eosinophils

A
  1. degrade eosinophilic major protein
  2. produce IL5
  3. produce eosinophil chemotactic factor
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35
Q

list the three types of polymorphonuclear cells (PMNC)

A
  1. neutrophils
  2. eosinophils
  3. basophils
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36
Q

are neutrophils APCs? what is the most prevalent leukocyte and in early phase of inflammation?

describe how neutrophils phagocytose and destroy pathogens

A

they are phagocytic but not antigen-presenting cell; most prevalent blood leukocyte and most prevalent in an early phase of inflammation

opsonization allows for neutrophils to phagocytose and destroy pathogens by allowing
1. chemotaxis
2. adherence
3. ingestion
4. destruction via ROS or NETS

37
Q

correlate the etiology of inflammation that is stereotypical for each type of PMNC

A

neutrophils - inflammation

eosinophils - parasite & immune-mediated

basophils - chronic inflammation, chronic (delayed) type hypersensitivity reactions, type I hypersensitivity reactions

38
Q

identify the two categories of innate lymphocytes and the functions of each

A

innate lymphocytes (ILC) protect barrier surfaces
1. cytotoxic - directly kill
2. noncytotoxic - do not directly kill

39
Q

list the types and locations of dendritic cells

A

dendritic cell precursor (bone marrow)
immature dendritic cells (tissues)
mature dendritic cells (lymphoid organs)

40
Q

describe dendritic cell activation, migration, and maturation

A

activation: local infection of tissues allows for complement activation, antimicrobial proteins/peptides, and phagocytes

migration: dendritic cells migrate to lymph nodes to allow phagocyte action/NK cell activation/cytokines & chemokine production to intiate adaptive immunity

maturation: the bacterial products, inflammatory mediators, cytokines and DAMPS allow dendritic cells to go from immature (tissues) –> mature (lymphoid organs)

41
Q

what are neutrophil extracellular traps (NETS)

A

highly activated neutrophils that result in a special cell death “NETosis” where neutrophils release de-condensed DNA/antimicrobial proteins (kamikaze mechanism where cell explodes and immobilizes/kills bacteria)

occurs in common sites of inflammation

all neutrophils are capable, but require certain amount of signal

42
Q

what are the targets of NK cells

A
  1. cells lacking MHC 1
  2. antibody-coated cells
  3. stressed cells
43
Q

what are heterophils?

A

similar to neutrophils but in rabbits, birds, and reptiles

44
Q

how do innate lymphoid cells (ILCs) differ from adaptive lymphoid cells

A

ILCs lack antigen receptors

Adaptive lymphoid cells will be antigen specific

45
Q

compare recognition of virus infected cells vs tumor cells by NK cells. How do NK cells kill their target?

A

virus infected cells - have an MHC I but are stressed
tumor cells - no MHC I

NK cells will kill with perforin, granzymes, cytokines, cell lysis

46
Q

list two possible causes of eosinophilic inflammation.

A
  1. parasites
  2. immune (e.g. allergic reactions)
47
Q

describe the features of inflammatory mediators

A
  1. pleiotropic (1+ functions)
  2. redundant
  3. synergistic
  4. antagonistic (inhibit others)
  5. cascade effects
  6. stereotypic response (not antigen specific)
  7. early stages of inflammation
  8. distrubuted widely but act locally
  9. rapidly inactive locally
  10. diverse chemical structure
  11. important mediators depend on species
48
Q

list the key activities of inflammatory mediators

A
  1. vascular effects (vasodilation/constriction, permeability, and endothelial effects on leukoyte migration)
  2. effect on leukocytes (chemotaxis & modulation of function)
  3. local & systemic effects (fever, pain, tissue damage)
49
Q

understand the roles of complement in innate immunity

A
  1. activation via pattern recognition trigger
  2. protease cascade amplification/C3 convertase
  3. effector mechanisms
    a. inflammation (C3a & C5a)
    b. opsonization for phagocytosis (C3b)
    c. membrane attack complex (MAC) (C5b)
50
Q

the major effects of kinins in inflammation

A

slow acting vasodilators
increase capillary permeability
mediate pain
produce rubor (redness), calor (heat) and dolor (pain) and swelling

51
Q

the major effects of vasoactive amines in inflammation

A

dilate arterioles
increase vascular permeability
e.g. histamine and serotonin (from mast cells)
*released early in inflammatory response

52
Q

the major effects of eicosanoids in inflammation
what do they come from
what enzymes are used
what are the 2 basic categories
examples

A

vasodilation/vasconstriction
increased vascular permeability
chemotaxis/adhesion
pain
resolution/repair

arachidonic acid
cyclooxygenases COX1 & COX2
housekeeping functions & inflamation/neoplasia
e.g. prostaglandins, thromboxanes, prostacyclins

53
Q

list the sources of inflammatory mediators

A
  1. cellular sources (mast cells, basophils, platelets, neutrophils, macrophages, lymphocytes, epithelium)
  2. tissues: liver *major source
54
Q

list the sources of inflammatory mediators

A
  1. cellular sources (mast cells, basophils, platelets, neutrophils, macrophages, lymphocytes, epithelium)
  2. tissues: liver *major source
55
Q

what is the role of C3 in complement

A

C3 convertase is the enzyme that creates C3a and C3b

56
Q

what is the role of C3b in complement

A

it acts as an enzyme to convert C5 into C5a and C5b

allows opsonization for phagocytosis and amplification of cascade

57
Q

what is the role of C3a & C5a in complement

A

release of histamine from mast cells to increase vascular permeability “anaphylatoxins” & chemoattractants for granulocytes & monocytes (neutrophils & macrophages)

58
Q

what is the role of C5b-9 in complement

A

form the membrane attack complex (MAC)

59
Q

list inflammatory mediators

A
  1. kinins
  2. vasoactive amines
  3. eicosanoids
  4. platelet activating factor
  5. ROS
  6. defensins
  7. lyosomal enzymes
  8. cytokines
  9. chemokines
60
Q

source & function of platelet activating factor (PAF)

A

source: inflammatory & endothelial cells
function: induce platelet aggregation, activates marginated neutrophils, increase vascular permeability, & bronchoconstriction

61
Q

source & function of reactive oxygen species

A

source: phagocytes
function: eliminates pathogens that have been phagocytosed

62
Q

source & function of defensins

A

source: animal and plant cells

function: active against bacteria, fungi & virsuses; assists in killing phagocytized bacteria by lysing the microbe
***peptides that embed in microbe membranes to form pore resulting in pathogen lysis

63
Q

source & function of lysosomal enzymes

A

source: mast cells, neutrophils, eosinophils, basophils, and macrophages
function: digestion of damaged tissues & pathogens; mediate inflammation

64
Q

source & function of cytokines

A

source: lymphocytes, monocytes, macrophages, leukocytes; formed via gene transcription

function: small proteins important for cell-cell communication

65
Q

source & function of chemokines

A

source:

function: small proinflammatory cytokines that have powerful chemotactic activity for neutrophils**; chemokine mix determines composition of leukocyte infiltration

66
Q

list cytokine families and key examples relevant to innate immunity/inflammation

A
  1. hematopoietin family: HSC differentiate into principle blood cells (RBC, platelets, macrophages, granulocytes, mast cells, T cells, B cells, NK cells) via JAK-STAT pathway
  2. IL-1 family (interlukins)
  3. interferon family
  4. tumor necrosis factor (TNF) family
67
Q

function of IL1

A

source: macrophages and many others

function: promotoes inflammation, affects leukocytes, kills tumor cells, affects brain (fever, drowsiness, appetite loss), affects cell growth, affects blood flow, affects metabolism
***fever, T cells, macrophage activation

68
Q

function of IL6

A

source: macrophages, T and B cells, dendritic cells, basophils, eosinophils, fibroblasts, keratinocytes, myocytes

function: T cells, hepatocytes, brain B cells
***acute phase protein production

69
Q

function of TNF

A

source: macrophages, monocytes, T cells, mast cells

function: promotoes inflammation, enhances fibroblast growth/collagen synthesis/bone resorption, toxic effects (sepsis), activates cells

70
Q

function of Type I Interferons (alpha & beta)

A

source: all cell types

function: inhibits translation, increases degradation, and inhibits RNA synthesis; affects viral protein trafficking, and stimulates antiviral immune responses & signals neighbor cells to put up barriers, signals infected cells to die, and recruits WBC to stimulate adaptive immunity

71
Q

function of Type II Interferons (gamma)

A

source: cytotoxic T lymphocytes and NK cells

function: induces expression of Fc and C3b receptors, stimulates NK cell activity, activates macrophages, enhances antigen processing/presentation

72
Q

list the events of acute inflammation

A
  1. capillary widening/increased blood flow via macrophage release of cytokines/chemokines = heat/redness
  2. increased capillary permeability/fluid release into tissues = swelling
  3. attraction of leukocytes (chemotaxis)/extravasation of leukocytes to site of injury = tenderness
  4. systemic response/fever and proliferation of leukocytes/release of inflammatory mediators = pain
73
Q

how do leukocytes exit the blood stream and enter the tissues

A
  1. rolling adhesion due to integrin (beta2) and intercellular adhesion molecule
  2. tight binding
  3. diapedesis (neutrophil changes shape and squeezes through due to chemokine concentration gradient)
  4. migration
74
Q

which leukocytes are present during an acute vs chronic immune response

A

acute: neutrophils

chronic: macrophage (more abdundant) and lymphocytes

75
Q

identify the source and diagnostic importance of acute phase proteins in different species

A

acute phase proteins: proteins during innate immunity that increase with infection and circulate the blood and participate in early phases of host defense against infection

  • in response to TNF, IL1 and IL6
  • vary between species and some are lectins and some are iron binding proteins
76
Q

what are the cause and effects of a cytokine storm

A

cause: PAMPs and DAMPs activate proinflammatory cytokines; massive systemic activation

effect: hypoxia, oxidant production, apoptosis, and necrosis leads to multiple organ failure

77
Q

how do damaged cells, inflammatory mediators and immune cells interact to cause inflammation

A
78
Q

what is the most common acute phase protein in all species

A

SAA which promotes inflammation via chemotaxis of monocytes, neutrophils and T cells

79
Q

cats mainly have what acute phase protein

A

AGP

80
Q

cows mainly have what acute phase protein

A

Hp

81
Q

pigs mainly have what acute phase protein

A

pig-MAP

82
Q

define primary pathogen

A

organism that frequently causes significant damage when invading a healthy individual

83
Q

define opportunistic pathogen

A

low virulence organism that causes damage in an immune impaired host

84
Q

list the non-cytotoxic innate lymphoid cells and their function

A

ILC1 - defense against viruses, intracellular pathogens
ILC2 - extracellular parasites and tissue repair
ILC3 - immunity to extracellular bacteria

85
Q

what is the function of NK cells

A

immunity against viruses and intracellular pathogens

86
Q

how are cytokines regulated

A

IL1 regulated antagonistically
TNF regulated via soluble receptor competing against cell membrane receptor

87
Q

what is a lymphokine

A

cytokine made by lymphocytes

88
Q

what is a monokine

A

cytokine made by monocyte/macrophage

Immunology (8 decks)

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