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A&P > A&P: Immune System > Flashcards

A&P: Immune System Flashcards

1
Q

Innate

A 
Nonspecific 
1st defense: skin and mucosal membranes
   Keratin
   Acid
   Enzymes
   Mucin
   Defensins
2nd defense:
   Phagocytosis
   Mast cells
   NK cells
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2
Q

Keratin

A

Resistant to most weak acids and bases and to bacterial enzymes and toxins

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3
Q

Mucin

A

Lines digestive and respiratory passages

Traps microorganisms and washes them out of the mouth into the stomach

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4
Q

Defensins

A

Output increases in response to inflammation when surface barriers are breached
Helps to control bacterial and fungal colonization in exposed areas

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5
Q

Phagocytes

A

Neutrophils, eosinophils, (monocytes) macrophages

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6
Q

Neutrophils

A

Most abundant

Becomes phagocytic on encountering infectious material in tissues

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7
Q

Monocytes

A

Leave bloodstream, enters tissues, and develops into macrophages

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8
Q

Free macrophages

A

Wander throughout tissue spaces in search of cell debris

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9
Q

Fixed macrophages

A

Permanent residents of particular organs

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10
Q

Mast cells

A

Release pro-inflammatory chemicals

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11
Q

NK cells

A

Natural killer cells

Go after foreign material (lyse and kill cancer cells and virus-infected body cells)

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12
Q

Inflammation

A

Red
Swelling
Pain
Heat

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13
Q

Effects of Inflammation

A

Prevents spread of damaging agents to nearby tissue
Disposes of cell debris and pathogens
Alerts adaptive immune system
Sets stage for repair

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14
Q

Opsonization

A

Own immune cells coat foreign material with opsin, so immune system can recognize it
Accelerates phagocytosis of pathogens
(When phagocytes are unable to recognize foreign matter)

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15
Q

Phagocytosis

A

Foreign material is identified
Neutrophils are 1st to show up, then macrophages
Macrophages can fight for longer period of time

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16
Q

Toll-like receptor (TLR)

A

Expressed in dendritic cells and macrophages
Innate immunity
Alert other immune cells to secrete pro-inflammatory chemicals

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17
Q

Pro-inflammatory chemicals

A 
Cytokines
Histamine
Kinin
Prostaglandin
Complement
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18
Q

Hyperemia

A

Increased blood supply or blood volume (increase of blood flow to area; more WBCs in area)

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19
Q

Exudate

A

Fluid that exits blood

Contains clotting factors and antibodies

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20
Q

Extravasation

A

Movement of WBCs from blood –> sites of tissue damage or infection

  1. ) Leukocytosis
  2. ) Margination
  3. ) Diapedesis
  4. ) Positive chemotaxis
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21
Q

Leukocytosis

A

Increase in # of WBCs
Leukocytosis-inducing factors: chemicals secreted during inflammatory response that induce proliferation of WBCs

Neutrophils enter blood from bone marrow

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22
Q

Margination

A

Neutrophil binds to endothelium of blood vessel
Dependent on CAMs
“Docks and rolls”

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23
Q

Diapedesis

A

Physical squeezing out of WBC through endothelium of blood vessel

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24
Q

Positive chemotaxis

A

WBC uses chemical signals secreted in inflammatory response (finds a way to area infected)

Migration up gradient of chemotactic agents

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25
Q

Interferons (IFNs)

A

Non-specific
Send warning to non-infected cells that there is a virus present
Inhibits virus from entering and/or replicating inside uninfected cell
Diffuse to nearby cells and stimulates synthesis of proteins that interfere with viral replication

Activate NK cells and phagocytes
NK cells physically bind

26
Q

Complement

A

Non-specific
Group of proteins
Activates inflammatory chemicals that amplify all aspects of inflammatory response

Enzymatic cascade
C3a: intensifies pro-inflammatory response
C3b: Helps assemble MAC (membrane attack complex)

27
Q

MAC

A

Cluster of different complement proteins that punches a hols into a bacterial plasma membrane

C3b binds to target surface and triggers insertion of MAC into cell membrane
When activated, kicks off MAC structure
Water flutes into bacterium and lyses it.

28
Q

Fever

A

Systemic response

  1. ) Macrophage ingests bacteria
  2. ) Endotoxins are released –> stimulation of phagocyte to secrete pyrogens

Pyrogens: IF-1, TNF-a
Stimlate prostaglandins in hypothalamus (resets thermostat; increases body temp)
Cell metabolism is increases (healing occurs faster)
Stimulates spleen and liver to hold Fe and Zn (low Fe and Zn in blood so less available to support bacterial growth)

29
Q

Adaptive

A 
Acquired
Specific
Systemic
Memory
3rd line of defense: must "meet" or be primed by an initial exposure to a specific foreign antigen
Chronic infections, cancers
Cell-mediated response: T cells
Antibodies (humoral) response: B cells
30
Q

Humoral Immunity

A

Extracellular pathogens
B cells/ Antibody-mediated
Antibodies present in body fluid bind to extracellular targets
Inactivating target temporarily and marking them for destruction by phagocytes or complement

31
Q

Cellular immunity

A

Intracelular pathogens

T cells

32
Q

Antigens

A

Provoke immune response
Ultimate targets of all adaptive immune responses
Self vs. Non-self
Proteins are the strongest antigen

33
Q

Clonal selection

A

B and T cells are activated
Then form clones specific to the antigens that activated them
Effector cells
Memory T and B cells

34
Q

Antigenic determinant

A

Part of the antigen that is immunogenic

35
Q

Epitope

A

Specific parts of antibodies that bind to specific antigens

36
Q

Immunogens

A

Complete antigens

Immunogenicity: can stimulate production of specific lymphocytes
Reactivity: can react with activated lymphocyte and antibodies released by immunogenic reactions

37
Q

Haptens

A

Incomplete antigens

Reactivity, but NOT immunogenicity
Part of foreign antigen combined with ones own protein
Only has immunogenicity when combined with a larger self-protein

38
Q

APC

A

Antigen-presenting cells

Engulf antigens, then present fragments of them on their own surfaces where T cells can recognize them

Dendritic cells: internalize antigen, enter lymph node and present antigen to T cell

Macrophages: presents to T cell, and also becomes activated by T cells in doing so

B cells: ONLY activate by helper T cells, after they have presented an antigen

39
Q

Self Tolerance

A

Recognize self from non-self
Must be relatively unreactive to self-antigens so that it does not attack the body’s own cells

Positive selection: specific to T cells; only T cells that recognize self-MHC proteins survive
Unable to recognize –> apoptosis

Negative selection: MHC carries self-antigens on it
Alerts immune cell that the antigen belongs in body
Ensures T cells do not recognize self-antigens displayed on self-MHC

40
Q

Clonal selection

A

An antigen binds to a particular lymphocyte that has a receptor for it and the antigen selects that lymphocyte for further development

41
Q

Plasma cell

A

Antibody-secreting cell
Effector cell
Humoral response

42
Q

IgG

A

Monomer

Predominates in secondary response

43
Q

IgM

A

Pentamer

1st antibody released in primary response

44
Q

Immunoglobulin

A

4 looping polypeptide chains
Linked together via disulfide bonds
2 identical heavy chains (flexible hinge region)
2 identical light chains

Antibodies responding to different antigen have very different V regions
C regions are the same in antibodies of the same class

45
Q

Fc

A 
Constant region
Same within members of the same family
Characterizes specific antibody
Genetic info
Stem region: where antibody binds to cell
46
Q

Fab

A

Antigen binding region

V regions of heavy and light chains combine –> antigen binding site

47
Q

Humoral Immunity: Memory

A

Primary response: 1st exposure to antigen
Lag time: 3-6 days
Peak plasma antibody at 10 days

Secondary response: any response after 1st
Lag time: short
Memory cell mount a rapid, strong response
Bind with greater affinity
Blood levels are high for weeks to months

48
Q

Active Humoral Immunity

A

Make own antibodies
Memory

Natural: infection (contact with pathogen)

Artificial: vaccine (dead/attenuated pathogens)
Whole cell
Subunit
Recombinant

49
Q

Passive Humoral Immunity

A

Borrow antibodies
No memory
Protection ends when antibodies naturally degrade in the body

Natural: antibodies passes from mother to fetus via placenta or to infant via milk

Artificial: injection of exogenous antibodies
Anti-toxin or anti-venom
Provides immediate protection, but effect is short lived

50
Q

Naive cells

A

CD4 T cells –> helper or regulatory

CD8 T cells –> cytotoxic

51
Q

Effector cells

A

Plasma cells: secrete antibodies

Helper T: helps activate B cells, other T cells and macrophages and direct adaptive response

Cytotoxic T: destroys any cells in the body that harbor anything foreign

Regulatory T: moderate immune response

52
Q

MHC proteins

A

Serve as receptors

Antigen presentation is necessary for both activation of naive T cells and normal functioning of effector T cells

53
Q

MHC class I

A

On surface of every nucleated cell
Healthy: display only endogenous antigens
Respond to cytotoxic T cell
Infected: endogenous antigens in combo with your and foreign antigens

CD8 T cells are activated by antigen fragments on class I

54
Q

MHC class II

A 
Less widespread
Only on surface of APCs
Exogenous antigens
Respond to helper T
CD4 cells are restricted to binding antigens only on class II
55
Q

TH

A

Help activate B and T cell immunity
Release cytokines

TH1
Stimulate inflammation, activate macrophages, and promote differentiation

TH2
Allergies and defend against helminth infections

56
Q

TC

A

Directly attack and kill other cells (lyse)
Main target: virus infected cells
Perforin
Granzymes

57
Q

Treg

A

Regulate activity of helper and cytotoxic T cells
Act by direct contact to by cytokines
Suppress/inhibit T cells when response is over
Help prevent hypersensitivity reactions and autoimmune disease

58
Q

Hypersensitivity

A

Antibody-stimulated

Cell-mediated

59
Q

Type I

A

Acute
Immediate

Helper T cells secrete IL-4
Plasma cells over secrete IgE
Release of too much histamine

Allergies/Allergen
Anaphylactic shock

60
Q

Type II

A

Subacute
Happens within minutes –> hours

Antibodies (IgG or IgM) binds to RBCs
Cytotoxic reaction

Happens in situations where blood or tissue is rejected
Can occur after a transfusion of mismatched blood

61
Q

Type III

A

Subacute

Autoimmune diseases
Intense inflammatory reactions
Accumulation of antigen-antibody complexes
Esosinophils aren’t destroying complexes –> buildup in tissues

62
Q

Type IV

A

Delayed (caused by T cells)

Macrophages secrete cytokine IL-12

Helper T and cytotoxic T cells over-proliferate and secrete additional cytokines
TC cells destroy other cells

Allergic contact dermatitis

A&P (10 decks)

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