Immune System Flashcards

1
Q

What is innate immunity?

A

present at birth and passed down genetically from the parents to children

Those were Ab’s originally created by the parent after fighting an infection

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2
Q

What is adaptive/specific immunity? 2 parts?

A

Response to a specific antigen => requires identification through memory cells

Cell-mediated immune system (T+B lymphos, monos, macros, dendrites, macros, etc)

Humoral immune system => Abs

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3
Q

What is passive immunity?

A

Transferring active humoral immunity in form of already made Abs either naturally (maternal=>placenta) or artificially when high levels of human Abs specific for a pathogen/toxin are transferred to non-immune individuals

=> short term

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4
Q

Def. of antigen?

A

Antibody generator => when induced stimulates production of Ab

=> can initiate CMI/humoral

Ag’s: Toxins, bacteria, foreign blood cells etc

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5
Q

What is an epitope?

A

Specific structural element on surface of the antigen recognized by a specific Ab

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6
Q

Greatest challenge of immune system?

A

Identify pathogen from self

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7
Q

What is clonal selection theory?

A

Born with vast variety of diff lympho’s based on genetic combination in early cell development
=> can react to Ag even for first ever encounter => proliferate/clone/mature for next time

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8
Q

Structure of IgX/Ab ? Which part binds to epitope of Ag ?

A

2 heavy chains/2 light chains bond by hydrophilic/phobic forces/disulfide bonds

Fc bind to pathogen
Fab binds to Ag(epitope)

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9
Q

What is opsonization?

A

Way of identification

=> Ab recognition/binding to bacteria, covering it
=> complement activation => bacterial lysis

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10
Q

Know structure/pic of all Immunoglob./Ab’s

A

K

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11
Q

Where is IgA found? What is special about it?

A

Dimer
15% of total
J chain marks it for secretion
Protects IgA from proteases <= secretory component

Secreted by B lympho’s in mucosal lining

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12
Q

IgD why is it special? Location?

A
Monomer
Produced by plasma cells (B lympho) 
1%
Co-expressed with IgM
Can activate B lymphos, baso,mast cells
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13
Q

IgE? Involved in? Structure? Abundance? Etc

A

Produced by plasma cells (B)

Involved in type 1 hypersensitivity allergic reaction and response to parasitic worms/protozoans
=> bind to Fc receptors found on surface of mast cells/basos

Least abundant

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14
Q

Most abundant IgG? Found where? Involved in? Special how?

A

Monomer
Produced by plasma cells/B lympho

Involved in types II and III hypersensitivity reactions and helps induce phagocytosis
=> only appears when prior infection happened (IgM) => 24-48h after Ag stimulation (time dependent)

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15
Q

Which Igs are found in human colostrum?

A

IgA most

IgG a lot too

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16
Q

IgM: structure/special/found where?

A

Large pentamer produced by plasma cells (B)
=> first Ab to appear

Spleen production, found in blood => blood type determination

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17
Q

What is hematopoiesis?

A

Formation of blood cellular components

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18
Q

All blood cells are produced from? Then differentiate by?

A

Haemotopoietic stem cell
=> common lymphoid progenitor =>lympho’s/plasma/dendritic

=> common myeloid progenitor =>Thrombo/Ery/Granulo=baso/neutro/eosino/mast cell

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19
Q

Types of lymphocytes?

A

B

T

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20
Q

Types of T cells?

A
Cytotoxic CD8
Th1
Th2
Suppressor T
Memory T
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21
Q

Types of B cells?

A

Plasma cells

Memory B cells

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22
Q

MHC function?

A

MHC acts as extracellular indicator of proper or dysfunctional intracellular protein balance

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23
Q

Function of class I MHC? Type of source?

A

Help mediate cellular immunity to address intracellular pathogens, such as viruses or destruction of malignant host cells

Endogenous source

=> recognized by CD8 coreceptor on Tc (=CTLs) or NKs

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24
Q

Class II MHC function?

A

Happens only on designated APCs (=macrophages, B cells, Dendrite cells) based on exogenous sources

=> TCR of naive helper T cells (Th0) has CD4 (cluster of differentiation 4) coreceptor that recognizes MHC II

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25
Q

What causes Abs to be produced?

A

B-cell with MHCII binds to Th0

=> B cell secrets Ig’s

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26
Q

Tc having CD8 recognize which type of MHC? On what kind of cells?

A

MHC I

Nucleated cells = not RBCs

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27
Q

Th cells having CD4 coreceptor recognize which MHC type? On what cell?

A

MHC II

=> APC

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28
Q

What is an APC?

A

Macrophage
DCs
Some B cells

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29
Q

How are pathogens processed inside the infected cell?

A

Host cell => present to T cell

Internal pathogen => digested into peptides by proteosome
=> taken up by TAP transporters (transporter associated with antigen processing) found in ER
=> into vesicles => cell surface => associate with MHC-I

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30
Q

How are pathogens processed outside a cell?

A
Taken up by specialized APCs => digest in lysosomes/proteasomes
=> peptide fragments => coupled with MHC class depending on size and moved to surface

=> express MHC-II (up to 14AA long)=>CD4=>Th

OR

=> express MHC-I (<8 AA long)

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31
Q

What activates MHC?

A

Binding of TCR to specific Ag-MHC complex => MHC signalling activated

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32
Q

First step of MHC activation? What is the goal?

A

Leukocyte-specific tyrosine kinase (LcK) with sarcoma homology domain binds cytoplasmic tail of CD4/8

=>=>=> altered gene expression=> T cell degranulation => Tc releases cytokines

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33
Q

Function of B-lympho in humoral immunity?

A

Differentiate into plasma cell upon Th2 activation => produce Ig’s

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34
Q

Function of Th cell?

A

Function in cell mediated immunity.

APC ingests antigen => presents to Th0 => differentiates into Th1/2

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35
Q

Function of Th2?

A

Th2 activates B cells / makes them proliferate

36
Q

Function of Th1?

A

Th1 activate Tc killing cells and phagocytes

37
Q

Which interferon of Th1 cells aids differentiation and making more Th1 cells?

A

IFN-y

Interferon-gamma

38
Q

Problem of HIV?

A

Gains entry via co-receptors and destroys/depletes CD4 T-cells

39
Q

What cells can act as APC?

A

Macrophages
DCs
B-cells

=> present to T cells

40
Q

After the T-cell has been presented an antigen from the APC, what are the two outcomes?

A

MHC-II/CD4/Th0 =>Th1/2/memory

MHC-I/CD8/Tc
Tc activated by Th1

41
Q

Function of suppressor/regulatory T cell (Treg)?

A

Acts to limit activation of immune system/phagocytosis

=> shut if off/tolerance to self

42
Q

Hypersensitivity is a result of?

A

Induction of indoleamine 2,3-dioxygenase = depletes tryptophan locally => prevent optimal function of Tcells

43
Q

Which cell can produce class switching from less efficient bigger IgM to IgG?

A

B-lymphos

44
Q

Tc and NK cells are similar in that they?

A

Attach infected cells/tumors by producing perforin/granulysin and granzyme ==> cell death

45
Q

Difference between NK and Tc cells?

A

Tc cells attack cells presenting foreign peptide

NK cells can attack without surface markers

46
Q

Phagocytic cell that can produce the cytokines IL-1 and TNF-beta?

A

Monocyte –diff–> Macrophage/DC

Either apparently produce cytokines, requires opsonization

47
Q

Phagocytic cells?

A

Monocyte, macrophage, neutrophil

48
Q

Primary marker of acute infection/inflammation and most abundant leukocyte?

A

Neutrophils

49
Q

How do neutrophils contribute in innate immunity?

A

Phagocytose

Release oxygen species/superoxides

Form neutrophil extracellular traps NETs => physical barrier/antimicrobial proteins/serine proteases

50
Q

Function of eosinophils?

A

Function in parasitic infections and allergies/asthma

Degranulation => major basic protein => parasites die

51
Q

Basophil function? Release?

A

Recruited to inflammation sites or parasites

Release anti inflammatories:
Histamine (promote blood flow)
Heparin (anti-clotting)
Proteolytic enzymes elastase/lysophospholipase
Leukotrienes
52
Q

How is histamine synthesized?

A

Histidine –decarboxylation–> Histamine + CO2

53
Q

Histamine’s function?

A

NT
Hormone => stimulate parietal cells to produce gastric acid
Allergic inflammatory reactions

54
Q

H1 histamine receptor?

A

Acts via Gq protein => phospholipase C/phosphatidylinositol pathway =>

Dilation/leakage of blood vessels
Motion sickness
Bronchoconstriction …

This is where most anti-histamines block receptors for allergies/motion sickness

55
Q

Characteristics of H2 histamine receptors?

A

On parietal cells => gastric acid

Target of GERD meds

56
Q

Characteristics of H3 histamine receptors?

A

Gi in CNS => inhibit release of NTs

57
Q

Characteristics of H4 histamine receptors?

A

Gi linked receptor => found in bone marrow and baso/mast cells

Majority found in nasal/oral mucosa

Involvement in IgE immune response

58
Q

How do dendritic cells recognize secreted molecules from bacteria/viruses?

A

Toll-Like Receptors TLRs

59
Q

Signals of APC + T cell binding?

A

1) MHC antigen presentation to TCR
2) binding of co-stimulatory molecules CD80/86 to CD28 (Tcell)
2+

60
Q

Which cytokines are both for acute inflammation and chronic inflammation?

A

IL1, 6, 11, 17,
TNF
Eotaxin
GM-CSF

61
Q

How are Type I/II cytokine receptors activated?

A

Janus Kinase JAK mechanism

62
Q

Ig receptors lead do?

A

Gene activation

63
Q

4 major cytokine receptor groups?

A

Type I/II

Ig

TNF

Chemokine

64
Q

Function of IL-1 alpha and beta?

A

Pro-inflammatory pyrogenic signal
Increases adhesion factors
Raise body temp

65
Q

Function of IL-2?

A

Th0 differentiation

66
Q

Which IL is involved in IgM-IgG class switching?

A

IL-4

Also increase production of MHC II

67
Q

Function of IL-5?

A

Induces eosinophils to increase IgA/G secretion

68
Q

Function of IL-6?

A

Increases differentiation of activated B lymphocytes into plasma cells => production of IgA/G

69
Q

Function of IL-10?

A

Inhibit antigen presentation/cytokine production

Stimulates maturation of T lymphos/mast cells/growth of B cells

Decrease CMI

70
Q

IFN-y function?

A

Inhibit viral replication

71
Q

APCs produce which cytokines?

A

IL-1, 12

72
Q

Th1 produces which cytokines?

A

IL-2
IFN
TNF

73
Q

Th2 produces which cytokines?

A

IL-4, 5, 6, 10

74
Q

What kind of response does HPV and Verruca cause?

A

IFN-alpha inhibition via gene expression (JAK-STAT)

75
Q

What is an autoimmune disease/immunosuppressant?

A

Loss of ability to distinguish self from non-self

76
Q

Two autoimmune diseases and drugs?

A

Myasthenia gravis
Goodpasture’s syndrome

Cylosporin/tacrolismus

77
Q

Treatment of autoimmune disorders?

A

Monoclonal antibodies (mimic body immune system) => interfere with CMI

78
Q

What is the complement system?

A

Helps/complements ability of Abs and phagocytic cells to clear pathogens

79
Q

3 complement pathways?

A

Classical
Alternative
Lectin

80
Q

Outcome and involvement of classic or alternative complement pathway?

A

Ag-Ab complex initiates, Lysis of cell is result by forming membrane attack complex MAC

81
Q

Difference between classic/alternative pathway?

A

Alternative pathway = first line of defense before immune response can start
Activated even in absence of Ab

Classic pathway is dependent on Ig binding to pathogen

82
Q

2 complement control proteins?

A

C3b promotes phagocytic ingestion

C5a chemotaxis

83
Q

Type 1 hypersensitivity reaction?

A

15-30min via IgE

Initial response by mast cells/basophils

84
Q

Type II hypersensitivity reaction?

A

Ab dependent CMI cytotoxicity

IgM/G by phagocytes/Kupffer cells/neutrophils

85
Q

Type III hypersensitivity reaction? Mech?

A

IgG/M, Ab, complement by Neutrophils/platelets

Time: 3-8h to weeks

Ag-Ab/complement => small blood vessels/joints/glomeruli => inflammation => tissue damage

86
Q

Type IV hypersensitivity reaction?

A

CMI or delayed

By Tc/Th1/monocytes

2-3 days +

TB, leprosy, histoplasmosis

87
Q

Transplant rejection types?

A

Hyperacute rejection - within minutes

Acute rejection - within a week

Chronic rejection - months to years