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MVST1B BOD > L2 - A Kelly - Immunity to infection > Flashcards

L2 - A Kelly - Immunity to infection Flashcards

1
Q

are commensals useful bacteria?

A

yep

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2
Q

Opportunistic pathogens rarely cause disease unless …

A

host defence is compromised.

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3
Q

5 points about the immune system

A
  • Constantly evolving
  • Protects us from infection and cancer
  • Network of cells products and tissues
  • Removes debris
  • Over 10% of human genes are involved in defence
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4
Q

innate infection reacts….

A

imediately

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5
Q

describe the barriers, cells and soluble components of the innate and adaptive immune systems

A
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6
Q

acute inflammation is ……

A

a stereotypic response to tissue injury (which can be sterile)

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7
Q

purpose of acute inflammation?

A
  • to eliminate the initial cause of cell injury,
  • remove damaged (necrotic) tissue resulting from the insult or the subsequent immune response
  • and to initiate repair of the damage tissue.
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8
Q

Picture for you

A
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9
Q

what are the activators of inflammation?

A
  • foreign / native soluble released factors
  • tissue damage
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10
Q

inflammation involves:

(2)

A

Recruitment of leucocytes to site of injury, and the release of inflammatory exudate

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11
Q

4 characteristics of inflammation

A
  1. Calour (heat)- from increased blood flow
  2. Dolor (pain)- stimulation of nerve ending
  3. Rubor (redness)- increased circulation/vasodilation
  4. Tumor (swelling)- increased fluid in the tissues
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12
Q

describe the physcial epithelial barriers of the immune system

A
  • Tight junctions between
    o squamous epithelial cells (skin)
    o mucosal glandular epithelia (GI & resp tract)
  • Cilia
  • Keratin
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13
Q

describe teh secretions of the epithelial barriers in the immune system

A
  • Mucous over glandular surfaces
  • Stomach acid (low pH)
  • Antimicrobial peptides (defensins, cathelicidins) damage microbe membranes.
  • Enzymes in tears and saliva (lysozyme) or stomach (pepsin)
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14
Q

can you remember the cell lines of teh immune cells?

A
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15
Q

the hematopoietic stem cells differentiates into

A
  1. common lymphoid precursor
  2. common myeloid precursor
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16
Q

which cells come from the common lymphoid precursor?

A

plasma cells

effector T cells

NK cells

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17
Q

which cells come fform the common myeloid precursor

A
  • Macrophages
  • Dendritic cells
  • Neutrophils
  • eosinophils
  • basophils
  • mast cells
  • platelets
  • erythrocytes
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18
Q

where to leukocytes come from?

A

generate in bone marrow by haematopoiesis

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19
Q

Monocytes mature into ____ in the _____

A

macrophages in the tissues

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20
Q

Mast cells resident in …..

A

connective and mucousal tissues

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21
Q

Describe neutrophils

A
  • Most abundant of all WBC
  • Follow chemotaxins C5a and fMLF
  • Phagocytose
  • Very short lived
  • Degranulate antibacterial proteins into ECF
  • can extrude their DNA forming neutrophil extracellular traps (NETs) to trap microbes (PUS).
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22
Q

describe macrophages:

A
  • phagocytose, and remove cellular debris
  • 2 types
    o M1: secrete cytokines and pro- inflammatory mediators that stimulate the acute inflammatory response.
    o M2 / alternatively activated: associated with tissue repair and parasite killing and expulsion.
  • Release cytokines to induce inflammation / repair
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23
Q

describe Mast cells

A
  • contain preformed mediators of inflammation such as histamine.
  • function is to rapidly induce inflammation.
  • Degranulate within seconds
  • A wide range of factors can induce degranulation including allergens (IgE), danger signals (PAMPs, DAMPs) and complement components (C3a, C5a), and substance P (neurogenic inflammation).
24
Q

what are sentinal cells

A

both mast and macrophages, when theyre beneath epithelial surfaces – sensing tissue damage

25
Q

describe eosinophils and basophils

A

non-phagocytic granulocytes providing defence against helminths worms and other parasites

26
Q

describe dendritic cells

A
  • Bridge adaptive and innate immune system
  • Recognise pathogens, drain to lymph nodes to start adaptive response.
27
Q

Describe NK cells

A
  • Important in viral infections
  • circulate in the blood in a partially activated state ready to respond immediately
  • kill infected cells and maintain or even increase the state of inflammation in infected tissue
  • recognise infected host cells by:
    • loss of self receptor expression on surface
    • expression of stress surface markers indicating cell is in stress
  • this is a balance between activating and inhibiting substances
  • in healthy cells – inhibitory substances dominate
28
Q

NK cells recognise infection and damage to cells using receptors that signal:

A

a. loss of molecules that normal cells express (missing-self)
b. expression of self molecules that are induced in stressed cells (induced-self)

29
Q

NK cells activation and inhibition balance:

A
30
Q

MHC class I molecules present …..

A

MHC class I molecules present peptide fragments, derived from cytosolic pathogens (eg viruses) to T cells, signalling that the virus infected cell should be killed

31
Q

describe how NK cells kill viral infected cells

A

infected cell produces cytokines (type I INFs)
induce resistance in surrounding cells
increase expression of ligands recognised by NK receptors
activate NK cells to kill
Macrophages produce CXCL8 and IL-12 to recruit NK cells and cause their proliferation
Activated NK cells produce cytokines (IFNγ) which activate macrophages and upregulate their killing capacity

32
Q

3 NK effector functions:

A
  • Degranulate perforin – holes in membrane
  • Bind Fc portion of antibodies – and kill cells attached with perforin.
    • Activated Fc receptor is strong – can activate the NK cell alone
  • Cytokines CXCL8 & IL-12 recruit and activate NK cells, which produce IFNγ which activates macrophages – increasing killing capacity, and initiates adaptive immune repsonse
33
Q

what are Innate Lymphoid Cells (ILCs)

A

function to amplify signals produced during innate recognition. The ILCs help orchestrate the early innate response.

34
Q

how any types of ICLs are there?

A

3

35
Q

describe ILC1s

A
  1. ILC1s protect against viruses and intracellular pathogens, they help activate M1 macrophage responses and may assist TH1 polarisation (similar to TH1 T cells see later).
36
Q

describe ILC2s

A
  1. ILC2s assist mucosal and barrier immunity against parasite and helminths infection, they indirectly help TH2 and M2 macrophage polarisation (similar to TH2 T cells see later).
37
Q

describe ILC3s

A
  1. ILC3s protect against extracellular bacteria and fungi (similar to TH17 T cells see later).
38
Q

Picutre

A
39
Q

describe cytokines

A
  • Small protein messengers
  • Bind to receptors on target cells
  • Low conc, shoert lived
    o Autocrine – same cell that secreted
    o Paracrine – nearby cells
    o Endocrine-like – distant cells
40
Q

4 characteristics that cytokines show

A
  • Redundancy, several different cytokines may have the same function
  • Pleiotropism, a single cytokine may have a variety of different effects
  • Antagonism, one cytokine blocks the action of another
  • Synergy, multiple cytokines work together to achieve an effect that is
  • greater than the additive effect of each alone
  • work through Jak/STAT signalling pathway
41
Q

Subgroups of cytokines?

A
  1. Interleukins
  2. interferons
  3. TNF family members
42
Q

describe histamine

A

Generated from histidine
Stored in granules in mast cells
Causes immediate capillary vasodilation.

43
Q

whats special about IL-8

A

IL-8 now renamed CXCL8 is a member of a subgroup of cytokines called chemokines. These are involved in controlling cell movement (chemotaxis).

44
Q

do some cytoines have systemic effects?

A

yep

45
Q

which cytokine shave systemic effects?

A

IL-6

C-reactive protein

46
Q

describe IL-6

A
  1. IL-6 stimulates hepatocytes to release acute phase proteins.
47
Q

describe C reactive protein

A
  1. C-reactive protein (opsonin and complement activation) and Fibrinogen (fibrin clot formation)
48
Q

decribe how fibrinogen can help limit bacterial growth

A

Fibrinogen is converted into insoluble fibrin strands. This can entrap bacteria limiting growth and dissemination and support the recruitment and activation of host cells facilitating elimination of infecting microbes.

49
Q

PROSTAGLANDINS AND LEUKOTRIENES =are….

A

PROSTAGLANDINS AND LEUKOTRIENES = potent inflammatory mediators

50
Q

describe teh production of certain arachodonic acid metabolites

A
51
Q

Describe the clotting system

A
  • Tissue damage
  • activates thrombin
  • converts fibrinogen to insoluble fibrin & fibrinopeptides.
  • Fibrin forms a clot to limit spread of infection.
  • Fibrinopeptides induce vascular permeability and neutrophil chemotaxis.
  • Thrombin cleaves both C3 and C5 -> C3a & C5a.
52
Q

describe teh Kinin system

A
  • Tissue damage
  • results in the generation of Bradykinin which increases vascular permeability, vasodilation, pain, smooth-muscle contraction.
    • The pathway activates complement components C3 and C5.
53
Q

describe teh fibrinolytic system

A
  • tissue damage
  • results in generation of Plasmin, a protease which degrades fibrin into products that recruit neutrophils (chemotactic).
  • Plasmin activates complement C3.
54
Q

describe teh complementn system

A
  • Complement cascades is activated by numerous mechanisms.
  • Results in opsonisation, membrane attack complex formation and generation anaphylatoxins (C3a, C4a and C5a)
55
Q

Fat

A

Mamba

MVST1B BOD (21 decks)

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