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pathophysiology > lecture 5 > Flashcards

lecture 5 Flashcards

1
Q

TNF-a

A
  • produced by activated macrophages
  • induced by LPS of gram - bacteria
  • mediator of acute inflammation - recruits neutrophils and macrophages to sites of infection
  • PRO-INFLAMMATORY
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2
Q

IL-1

A
  • produced by activated macrophages
  • similar to TNF-a but also helps activate T-cells
  • PRO-INFLAMMATORY CYTOKINE
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3
Q

IL-10

A
  • produced by activated macrophages and TH2 cells (CD4)
  • inhibits cytokine production by activated macrophages, expression of MHC II and co-stimulatory molecules on macrophages and inhibits production of IFN-y by T-cells which shifts immune response from attack to repair functions
  • INHIBITORY CYTOKINE (dampens immune response)
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4
Q

IL-12

A
  • produced by activated macrophages and dendritic cells
  • stimulates IFN-y and induces differentiation of Th cells to become Th1 cells
  • enhances cytolytic functions of Tc and NK cells
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5
Q

TH1

A
  • cell-mediated immunity and inflammation
  • intracellular pathogens (viruses, bacteria)
  • autoimmunity
  • inflammation

IL-12 , IFN-y –> IL-2, IFN-y, TNF-a

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6
Q

TH2

A
  • antibody-mediated immunity
  • promotes humoral immunity (B)
  • extracellular parasites
  • asthma, allergy

IL-2, IL-4 –> IL-4, IL-5, IL-6, IL-10, IL-13

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7
Q

TH17

A
  • extracellular bacteria (skin, lining of intestine)
  • promotes innate immunity
  • fungi
  • autoimmunity

IL-6, TGF-B –> IL-17, IL-21, IL-22

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8
Q

Treg

A
  • immune tolerance
  • lymphocyte homeostasis
  • regulation of immune responses
  • control/ dampen immune response (inhibits adaptive response)
  • maintain tolerance to self antigens
  • prevent autoimmune disease

do this by: inhibitory cytokines, cytolysis, targeting dendritic cells, metabolism disruption

IL-12, TGF-B –> TGF-B, IL-35, IL-10

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9
Q

TH0

A

Naieve T-cell

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10
Q

TH1 response

A

cell-mediated, intracellular attack

cytokines lead to:
- macrophage activation (enhanced microbial killing)
- complement-binding and opsonizing antibodies
- neutrophil activation (enhanced microbial killing)

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11
Q

TH2 response

A

humoral focus

  • production of neutralizing IgG antibodies
  • production of IgE (mast cell degranulation)
  • suppression of macrophage activation
  • eosinophil activation

*TH1 and TH2 counter eachother

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12
Q

T-cell activation –> naieve effector –> memory cells

A

initiation (naieve) –> clonal expansion (effector cells) –> contraction –> maintenance (memory cells)

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13
Q

IL-1 and IL-6 and TNF-a are important in…

A

inflammation (pro-inflammatory?)

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14
Q

how do immune cells exit circulation?

A

selectin -
integrin -
help get immune cells to exit circulation into tissue
ICAMs -

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15
Q

IL-2

A

inflammation and proliferation

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16
Q

membrane TLRs

A

ex. LPS can’t get into cell (fragments of bacteria)

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17
Q

endosome TLRs (from endocytosis, virus was sucked up into the cell)

A

ex. more viral things

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18
Q

PRRs (DAMP/ PAMP expression)

A
  • TLRs
  • RLR (rig-like-receptor) - IFNa/B (look for viral RNA)
  • NLR (NOD-like-receptor) - inflammatory, cytoplasm
  • lectin like receptors - surface, recognize funguses

*expressed in various compartments where they will potentially encounter their ligands

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18
Q

etc..

A
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19
Q

sentinal cells

A

DCs, macrophages, NKs all over lots near surface

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20
Q

anti-viral response

A

type 1 interferons

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21
Q

is complement a primary response?

A

no, it’s later

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22
Q

APCs

A

macrophages, dendritic cells, B-cells

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23
Q

TLR1: TLR2

A

bacterial lipopeptides

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24
Q

TLR2

A

bacterial peptidoglycan

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25
Q

TLR4

A

LPS (gram-)

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26
Q

TLR5

A

bacterial flagellin

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27
Q

TLR2: TLR6

A

bacterial lipopeptides

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28
Q

extracellular TLRs

A

1,2,4,5,6

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29
Q

endosomal TLRs

A

3,7,8,9

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30
Q

TLR3

A

dsRNA

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31
Q

TLR7

A

ssRNA

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32
Q

TLR8

A

ssRNA

33
Q

TLR9

A

CpGDNA

34
Q

TLR6

A

lipoteichoic acid

35
Q

sentinal cells

A

DCs, macrophages, NK cells (waiting for attack)

36
Q

circulating phagocytes and granulocytes

A

recognize groups of pathogens (could be recruited to sites)
- neutrophils, monocytes, eosinophils, basophils

37
Q

blood proteins

A

complement, mediators of inflammation

38
Q

cytokines

A

coordinate signals, turn on and build up immune response

  • signal, stimulation, regulation of immune response
39
Q

(make flashcards for lec 3 and 4,5,6 and then go over all of them and summary sheet every night)

A
40
Q

features of innate immune system

A

fast
general
no diversity or specificity
no memory
first line of defense

41
Q

features of adaptive immune system

A

slower
specific and specialized
diverse
memory
offers selective and precise protection

42
Q

constant region of Ig (Ab) - ex. IgG, IgM, IgD is bound by…

A

macrophages

or recognized as a tag

all sticks (constant regions) are the same

43
Q

antigen binding site

A

specific to one antigen (variable regions) unique to each cell

44
Q

Thf

A

promotes B-cell differentiation

45
Q

steps of adaptive immune response

A

antigen recognition –> lymphocyte activation –> antigen elimination –> contradiction (homeostasis) –> memory

46
Q

regulation of immune response

A
  • Treg
  • Inhibitory/ regulatory cytokines (IL-10)
  • whatever is turned on needs to be turned off
  • neg feedback loops
  • TLRs
    -NKs
  • MHC I and II
47
Q

pleiotropy cytokine

A

1 cytokine can have different effects on different cells

48
Q

redundancy cytokines

A

go from one cell to many

proliferation of different cytokines (IL-1, IL-4, IL-5) can all produce proliferation in B-cell

49
Q

cascade induction cytokines

A

might have one T-helper cell (CD4) –> cascade –> produces other activated Th cells

50
Q

antagonism cytokines

A

inhibition, some cytokines inhibit other cytokines

51
Q

synergy cytokines

A

2 cytokines work together (ex. IL-4 and IL-5) to activate B-cells

52
Q

compartmentalization of immune system tissues

A
  1. circulating system (blood and lymph) - 2%
  2. organ system (98%)
    primary: central lymphoid organs: bone marrow (B-cells maturation) and thymus (T-cell maturation)
    secondary: peripheral lymphoid organs: lymph nodes, spleen, mucosal-associated lymphoid tissue (gut)
53
Q

4 immune privilages sites

A

CNS, Placenta/ fetal unit, testes, eyes (susceptible to loss of function by inflammation)

characterized by:
- low or lack of MHCI expression in tissues
- inhibiting surface molecules and cytokines
- lack of systemic lymphatic drainage
- cellular barriers that block immune cell entry
- sites tend to contain their unique immune cells that do not cause inflammation or induce immune suppression (specialized macrophages/ Treg cells)

54
Q

3 stages of existence for macrophages

A
  1. resting “lie and wait” “patrolling mode”
  2. activated/ primed by cytokines IFNy - Antigen presentation mode
  3. hyperactivation “destroyer mode”
55
Q

lifespan of neutrophils

A

short - 5-7 days

56
Q

outcomes of inflammation

A
  • vasodilation/ increased blood flow
  • fluid accumulation
  • chemical activation/ cytokine release
57
Q

chemical mediators of inflammation do…

A

intensify inflammatory response
- ex. mast cells, histamine, prostaglandins, leukotrienes, bradykin, complement

58
Q

2 types of type 1 interferons

A

(immune cells, fibroblasts, endothelial cells)
- interferon a) mostly dendritic cells, macrophages
- interferon B) a wide range of cells

antiviral properties: inhibit viral replication/ transcription on ADJACENT cells (paracrine action)

59
Q

additional roles of type 1 interferons - adaptive priming

A
  • sequestration of lymphocytes in lymph nodes (maximize encounter)
  • increase cytotoxicity of killers
  • upregulate expression of MHC1
60
Q

ANTIGEN (can be made of…)

A
  • protein or carb
  • proteins
  • polysaccharides
  • lipids
  • nucleic acids
61
Q

epitope

A

part of an ANTIGEN that immune system recognizes
- interacts with antibody or T-cell receptor

  • one antigen can have many epitopes
62
Q

general features of DCs

A
  • immature/ quiescent state
  • mature state (once STIMULATED through PRR) main goal to present antigen to naieve T cells and activate them
63
Q

3 necessary elements to activate a T-cell

A

signal 1: MHC-peptide-TcR recognition (naive and memory T-cells)

signal 2: CO-STIMULATION recognition (naive T-cells)

signal 3: cytokine signalling recognition (naive and memory cells)

64
Q

how can naive antigen-specific lymphocyte contact it’s specific antigen?

A

dating bars of the body - LYMPH NODES

65
Q

secondary lymphoid organs

A
  • lymph nodes
  • spleen (blood)
  • GALT (gut) lamina propria, peyer’s patches
  • BALT (respiratory)
  • MALT (mucosal lymphoid tissue/ gut)
66
Q

langerhans cells (immature DCs in skin)

A

once they encounter antigen, they can enter lymph node and transfer Ab to other DCs which will be able to present these to B-cells

67
Q

roles are CD4 are terminal?

A

no! can change with course of infection

68
Q

memory cells can be…

A

B or T cells

69
Q

(more detailed stuff in lecture 6 to check)

A
70
Q

pos and neg selection

A

pos: select for recognized MHC

first recognize MHC I or II or dont, if you don’t then kill

neg:
select against self antigens
next, if you recognize as self, it is killed

71
Q

HLAs of MHC 1

A

HLA A,B,C

72
Q

HLAs of MHC II

A

HLA DP, DQ, DR

73
Q

main property of MHCs

A

polymorphic

74
Q

most variable HLAs

A

HLA-A, HLA-B, HLA-DR

75
Q

how are T-cell receptors made?

A

VDJ recombination - gives diversity

TcRs have 1 antigen binding site whereas BcRs have 2

76
Q

each T-cell is unique!

A

yes

77
Q

dendritic cell vs macrophage (short-lived vs long-lived)

A

DC = short lived (primary APC)
macrophage = long lived

78
Q

what do PRRs do

A

most important to turning on APCs

TLRs help turn on co-activation to get process going (innate)
- TLRs are on B-cells, macrophages, and DCs (APCs)

79
Q

CD8 T-cells need to be activated TWICE

A
  1. use MHC receptors to activate/ turn on from dendritic cells (co-activation)
  2. destroys cells now

*remember, all cells express MHC1

80
Q

CD4 cells can respond to both innate and adaptive controls T/F

A

true (macrophages, NKs, CD8, B-cells)

pathophysiology (10 decks)

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