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Principles (Y1) > Immunology > Flashcards

Immunology Flashcards

1
Q

How does the immune system identify harmful organisms

A
  • by distinguishing self from non self proteins

- identifying danger signals (eg from inflammation)

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2
Q

what occurs when the immune system goes wrong?

A
  • allergies
  • recurrent infections
  • autoimmune disease
  • cancer
  • transplant rejection
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3
Q

What is veriolation

A

immunisation where the same organism is admin as the disease–> causing organism but the route of admin is different
eg exposure of an individual to the contents of dried smallpox from an infected patient

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4
Q

What is immunisation

A

when one disease may protect against another by cross reactive antibodies that neutralise the other infection too

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5
Q

What is the unequal battle between host and pathogen?

A

pathogens evolve alot faster than hosts, host have to rely upon a flexible and rapid immune response, with a degree on non-specificity

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6
Q

Barriers to infection: SKIN

A

SKIN- physical barrier (tight packed cells), physiological barrier (low pH), sebaceous glands (secrete hydrophobic oils, lysozymes, defensins, ammonia) low O2 tension, cells undergo renewal

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7
Q

Barriers to infection: MUCOUS

A

Physiological barrier, secretory IgA, enzymes (lysozymes, defensins, antimicrobial peptides directly killing pathogens, lactoferrin acts to starve invading bacteria of iron) cilia (trap pathogens and revove mucous)

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8
Q

Barriers to infection: COMMENSAL BACTERIA

A

compete with pathogens for scarce resources and produce fatty acids and bactericidins that inhibit the growth of pathogens

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9
Q

What are first line defences?

A

physcial barriers

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10
Q

what are second line defences?

A

immune barriers

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11
Q

what is the innate immune system?

A 
rapid response (0-4h)
general response
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12
Q

what cells does the innate imune response involve?

A

-mast cells
-NK cells
-phagocytes
-complement
these are responsible for acute inflammation and killing of pathogen

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13
Q

what is the adaptive immune response?

A 
slow response (4-96h)
unique response- immunological memory
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14
Q

what cells does the adaptive immune response involve?

A

antigens

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15
Q

Cell components of the immune system?

A

PHAGOCYTES (neutrophils, monocytes, macrophages, dendritic cells) ingest and kill bacteria, important source of cytokines
LYMPHOCYTES (T cells, B cells, natural killer cells)
EOSINOPHILS, MAST CELLS AND BASOPHILS

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16
Q

Soluble components of the immune system?

A 
ANTIBODIES (immunoglobulins- produced in response to antigens)
COMPLEMENT PROTEINS (produced in the liver, critical role in inflammation and defence, complement cascade)
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17
Q

name 3 Haemotopoietic stem cells

A

Common lymphoid progenitor
Common myeloid progenitor
Common erythoid megakaryocyte progenitor

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18
Q

Common lymphoid progenitor function:

A

differentiate into lymphocytes

NK/T precursors develop in the thymus

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19
Q

Common myeloid progenitor function:

A

Differentiate into phagocytes, basophils, eosinophils and mast cells

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20
Q

Common erythoid megakaryocyte progenitor function:

A

differentiate into platelets and erythrocytes

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21
Q

Mast cells:

A
  • reside in tissues and protect mucosal surface
  • degranulates and releases trypsin and tryptase
  • gene expression- TNF, chemokines and leukotrines
  • fight parasites
  • allergic reactions
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22
Q

Basophils and eosinophils:

A
  • circulate in blood
  • recruited to sites of infection
  • fight parasites
  • allergic reactions
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23
Q

Phagocytes:

A

ingest and kill bacteria and fungi, also clear debris from dead tissue cells and produce cytokines that will promote and acute inflammatory response

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24
Q

Neutrophils:

A
  • circulate in blood
  • rapidly recruited to inflammed and infected tissues
  • short lives professional killer cells
  • PAMP recognition and activation
  • active neutrophils produce TNF
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25
Q

PAMP AND PRR

A

The innate immune system constitutes the first line of defense against invading microbial pathogens and relies on a large family of pattern recognition receptors (PRRs), which detect distinct evolutionarily conserved structures on pathogens, termed pathogen-associated molecular patterns (PAMPs).

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26
Q

how do neutrophils attack pathogens?

A

Phagocytosis
release of antimicrobial peptides and degradative proteases
generate extracellular traps

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27
Q

what does dead neutrophils+tissue cells+ microbial debri=?

A

PUS

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28
Q

Lysosomes in neutrophils:

A
  • contain toxic reactive species (oxidative killing), hydrolytic enzymes and acidic pH that makes them good at killing pathogens
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29
Q

Monocytes:

A
  • monocytes are precursors of macrophages
  • limit inflammation
  • involved in tisue repair and healing
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30
Q

Macrophages:

A
  • reside in tissues
  • ingest and kill extracellular pathogens
  • clear debris from dead tissue cells
  • inflammation
  • tissu repair and would healing
  • antigen presentation
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31
Q

Dendritic cells:

A
  • immature cels in peripheral tissues
  • when in contact with a pathogen they mature and migrate to secondary lympoid tissues
  • stimulate adaptive immune response
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32
Q

Natural killer cells:

A
  • large granular lympocytes
  • specifically kill tumour and viral infected cells
  • can also kill anti-body bound cells
  • kill by realsease lytic granules
  • release a cytokine gamma-INF which engances macrophage killing activities
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33
Q

T and B cells:

A
  • Mature cells constantly circulate through blood, lymph and secondary lympoid tissues and are activated when they meet a pathogen
  • long lived T and B cells are known as memory cells
34
Q

T cells:

A

defence agains pathogens

  • Helper T cells (regulators of the immune system and activate other immune cells - CD4+)
  • Cytotoxic T cells (kill virally infected body cells- CD8+)
35
Q

B cells:

A

produce antibodies

36
Q

What happens in primary lympoid tissues?

A

site of leukocyte development (bone marrow and thymus)

37
Q

What happens in secondary lympoid tissue?

A

site where adaptive immune responses initiate (tonsils, spleen, lymph nodes)

38
Q

function of lymph nodes?

A

remove pathogens and antigens from lymph

39
Q

Direct contact of the immune system?

A

receptor- ligand interactions

40
Q

indirect contact of the immune system?

A

production and secrettion of cytokines

41
Q

Cytokines

A
  • produced in response to infection, inflammation and tissue damage
  • produced in injured tissue cells and activated immune cells
  • short half life
  • can cause fever via the hypothalamus
  • co-ordinate the immune system by modulating cell behaviour
42
Q

Cytokine signals:

A 
Autocrine signals (for self)
paracrine signals (for near by cells)
signals for distant cells
43
Q

Examples of Cytokines

A

INTERFERONS: anti-viral functions
TNF: tumour necrosing factor, pro-infammatory
CHEMOKINES:control and direct cell migration
INTERLEUKINS:
IL1 AND IL6= proinflammatory
IL2 = T cell proliferation
IL10= anti inflammatory

44
Q

aim of the innate immue response

A

acute inflammation and killing of pathogens

45
Q

Recongition phase in the innate immune response:

A

PRRs (pattern recognition receptors)
-PRR toll like receptor 4 is found on the cell surface- this find the lipopolysaccharide PAMP
-PRR Detectin 1 is found on the cell surface- find the B-glucans
-PRR NOD2 is found intracellularly- find the muramyl dipeptide
-PRR toll like receptor 7 is found intracellularly- find ssRNA
PAMPs (pathogen associated molecular patterns) (neutrophils uses this for recognition and activation)

46
Q

Activation phase of the innate immune response:

A

inflammation and pathogen killin

47
Q

Pro-inflammatory effects of histamine from mast cell degranulation:

A
  • increased vascular permeability
  • vasodilation
  • activation of endothelial cells
  • pain
48
Q

Pro-inflammatory effects of tryptase from mast cell degranulation:

A

-proteolytic enzyme

49
Q

Pro-inflammatory effects of TNF from mast cell degranulation:

A
  • increased vascular permeability

- activation of endothelial cells

50
Q

Pro-inflammatory effects of leukotrenes from mast cell degranulation:

A
  • smooth muscle contration

- increased vascular permeability

51
Q

Pro-inflammatory effects of chemokines from mast cell degranulation:

A

-attract other innate immune cells

52
Q

Acute phase reponse:

A

liver produces acute pahse proteins in repsonse to pro-inflammatory cytokines (IL1, IL6 + TNF)

  • increased vascular permeability
  • activation of endoethelial cells
  • increased neutrophil production and mobilisation
53
Q

Molecules expressed on active endothelial cells at sites of inflammation:

A 
ACHESION MOLECULES (SELECTINS AND ICAMS)- allow leukocytes to bind weakly to endothelial cells and roll slowly along endothelial surface
CHEMOKINES then activate the leukocyte so that they can bind more strongly to the endothelial cell- integrins on the leukocyte then bind to the ICAMs on the endotheilial surface
Once inside the cel the leukocytes follow a chemokine gradient to get to the site of infection
54
Q

Leukocyte adhesion deficency:

A

rare genetic disease defined by a loss in B2 integrins causing defective transendothelial migratoin. ie leukocytes cannot leave the bood stream and infections cannot be cured

55
Q

Phagocyte defiency disease:

A

CHRONIC GRANULOMATOUS DISEASE: recurrent bacterial and fungal infections

56
Q

Phagocyte defiency disease:

A

CHRONIC GRANULOMATOUS DISEASE: recurrent bacterial and fungal infections

57
Q

Complement System

A

Family of proteins produced in the liver that circulate in the blood
Enter infected and inflamed tissues

58
Q

3 pathways of the complement system

A

Classical pathway- antigen-antibody complexes
Lectin pathway- mannose binding lectin (MBL) binds to certain sugars on the pathogens surface
Alternative pathway- amplification loop which causes the spontaneous breakdown of C3–>C3b+C3a (positive feedback)

59
Q

Functions of the complement system

A
  • Membrane attack complex
  • Opsonisation(Coating of microorganisms by immune proteins (opsonins) EG, C3b, CRP, antibodies…Enhances phagocytosis)
  • Chemotaxis
  • Clearance of immune complexes
  • Inflammation
60
Q

4 complement inhibitors

A

C1 Inhibitor, Factor I, Factor H and C4 binding

61
Q

antigens

A

(communication between pathogen and leukocyte)

Cause adaptive immune response by activating B and T cells

62
Q

T cells recognise pathogen by

A

T cell antigen receptor = membrane-bound protein heterodimer (Has alpha and beta chain)

63
Q

B cells recognise pathogen by

A

B cell antigen receptor = membrane bound antibody (IgM or IgD) (Has light and heavy chain and disulphide bridges. Membrane bound and soluble proteins)

64
Q

HLA/ MHC

A

The human leukocyte antigen (HLA) system or complex is a gene complex encoding the major histocompatibility complex (MHC) proteins in humans. These cell-surface proteins are responsible for the regulation of the immune system in humans.

65
Q

MHC/HLA proteins display peptide antigens to T cells

A

Class 1 - expressed on all nucleated cells - present peptide antigens to cytotoxic T cells
Class 2 - expressed only on dendritic cells, macrophages, B cells - present peptide antigens to helper T cells

66
Q

Stromal cells:

A

found in B cell zones and trop opsonised antigens

67
Q

Stromal cells:

A

found in B cell zones and trop opsonised antigens

68
Q

Antibodies

A
  • Immunoglobulins
  • Produced by B cells in response to an antigen, bind specifically
  • Provide defence against extracellular pathogens
  • Each heavy and light chain contains a variable region and a constant domain
  • Variable regions - antigen binding sites
69
Q

what antibodies do mothers pass onto their children?

A

IgG and dimeric IgA

70
Q

what antibodies found on B cell membranes as B cell antigen receptors

A

IgM and IgD

71
Q

Recognition function of antibodies

A

Binding to antigen mediated by variable region sites

72
Q

Effector function of antibodies

A

Clearance mechanisms mediated interaction of Fc constant region with effector molecules (Complement molecules and Fc receptors)

73
Q

Agglutination

A

Immune complex formation

74
Q

antibodies can function as opsonins:

A

phagocytes have FC receptors and therefore bind to the Fc region of immunoglobulins which are circling the pathogen, enhancing phagocytotic clearnace

75
Q

antibodies can stimulate NK cells:

A

have FC receptors too and so bind to antibody bound to the pathogen

76
Q

antibodies can trigger allergic responses:

A

mast cells have Fc receptors which bind to Fc on antibody and causes mast cell degranulation

77
Q

germinal centre

A

Germinal center are sites within secondary lymphoid organs – lymph nodes and the spleen[1] where mature B cells proliferate, differentiate, and mutate their antibody genes, and switch the class of their antibodies (for example from IgM to IgG) during a normal immune response to an infection.

78
Q

germinal centre reactions

A
  • B cell proliferation
  • Antibody heavy chain switching
  • Generation of high affinity antibodies
  • Differentiation into Plasma cells and Memory B cells
79
Q

IL2

A

helper T cells produce these to increase proliferation of bother helper T cells themselves and Cytotoxic T cells- once helper T cells have migrated to the site of infection and inflammation they are reactivated by marcrophages

80
Q

Somatic hypermutation

A

to produce antibodies that recognise the same antigen but with increased affinity, achieved by point mutation made in the heavy light chain gene segments

81
Q

IgG

A

is the secondary response to antigens

Principles (Y1) (9 decks)

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