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EMS - MOD > week 3 > Flashcards

week 3 Flashcards

1
Q

give me three examples of innate immune response?

A

patter recognition receptor, cellular ( phagocytes, NK cells) physical and chemical barriers/ mechanism

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2
Q

give me 2 examples of adaptive immune response?

A

humoral and cellular

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3
Q

what is pattern recognition receptor? give examples?

A

Inclusive term for antigen recognition receptor in innate system
Each immune cell carries identical receptor of a given type
Examples are
Toll-like receptors (TLR’s), NOD-like receptoes (NLR’s), RigI-like receptors (RLR’s) C-type lectins (CLR’s), scavenger receptors

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4
Q

what do cytokines do?

A

they are chemicals that tell the immune system what to do

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5
Q

what are the two groups of pattern recognition receptors?

A 
Cell surface (transmembrane) and intracellular receptors – TLRs, NLRs, RLR’s and CLR’s
Fluid-phase soluble molecules
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6
Q

What is the first cytokine you produe in response of infection?

A

IL-1 –> fever like symptomes but allows the rest of the immune system to engage

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7
Q

What are the two fluid phase recognition molecules?

A

Mannan-binding Lectin

Surfactant Protein A & D

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8
Q

What is the process and function of fluid phase recognition

A

Recognition of microbial complex carbohydrates

Bind via Carbohydrate-Recognition Domains (CRDs) –> sugars or combination of sugars and protein on the surface of the bacteria
Role in neutralisation of pathogen
Role in recruitment of adaptive response

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9
Q

how is the classical pathway activated?

A

antigen antibody interaction

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10
Q

how is the MB-lectin pathway activated?

A

the mannose binding lectin binds to the lectin on the surface of the pathogen

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11
Q

how is the alternative pathway activated?

A

on the pathogen surface

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12
Q

what do TNF and IL-6 instruct?

A

they tell what the immune system should do such as T cells

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13
Q

what do macrophages do?

A

bind and kill bacteria –> APC –> produce and bind to inflammatory cytokines

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14
Q

what are the role of Plasmacytoid dendritic cells (DCs)?

A

Produce large amounts of interferon- (IFN-) which has antitumor and antiviral activity, and are found in T cell zones of lymphoid organs; they circulate in blood.

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15
Q

what is the role of Myeloid dendritic cells?

A

produce IL-12 and IL-10 and are located in T cell zones of lymphoid organs, circulate the blood and present in the interstices of the lung, heart, and kidney.

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16
Q

what do eosinophils do?

A

kills invading parasites

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17
Q

what do Neutrophils do?

A

Phagocytose and kill bacteria, produce antimicrobial peptides

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18
Q

what do Mast cells and basophils?

A

Release TNF-, IL-6, IFN- in response to a variety of bacterial PAMPs (pathogen associated molecular pattern)

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19
Q

what is the contribution of epithelial cells to the immune system

A

produce antimicrobial peptides–> tissue specific epithelial produce mediators of the local innate immunity

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20
Q

what is clonal expansion?

A

the Proliferation of chromosomes in response to a infection –> the one with the corrrect receptor will carry on ploriferating

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21
Q

what are the name of the two regions of the receptor on B and T cells

A

FC region that is variable region and FAB region –> constat region

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22
Q

give example of Antigen presenting cells

A

macrophages, B cells and dendrites

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23
Q

what cells are MHC class 1 found on? What are the 3 HLA’s found on class 1

A

Found on all cells

Classes –> HLA-A , HLA-B, HLA-C

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24
Q

what cells are MHC class 2 found on?

What are the 3 HLA’s found on class 2

A

On antigen presenting cells such as dendritic cells, macrophages, some endothelial cells, thymic epithelial cells, and B cells.

Classes–> HLA-DP, HLA,DQ and HLA-DR

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25
Q

which T cell type does MHC class 1 present too?

A

They present the antigen peptides to cytotoxic T cell

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26
Q

what T cell does MHC class 2 present peptides too?

A

They present the antigen peptides to T helper cells

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27
Q

what is suppressor T lymphocytes?

A

help to dappen down immune response

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28
Q

what are Helper T cells?

A

secrete growth factors (cytokines) which control immune response: Help B lymphocytes and T lymphocytes (Helper T cells are target of HIV)

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29
Q

what are the types of invactivation of a antigen by a antibody?

What do they lead onto?

A

neutrilization –> blocks viral binding sites –> coats bacteria
agglutination of microbes
precipitation of dissolved antigens

These 3 enhance phagocytosis

activation of the complement system which leads to cell lysis

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30
Q

What is the outcome when dendritic cells activate Th1 CD4+ T cells

A

Induce CD8 cytotoxic T cells which kill microbe infected cells
B cell and IgG antibody which opsonise microbes for Phagocytosis
macrophage activation –> kills opsonized microbes

Inhibit the TH2 pathway

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31
Q

What is the outcome when dendritic cells activate Th2 CD4+ T cells

A

Eosinophill–> Kill parasite
mast cells basophils
B cells that produce IGM
IGG IGA and IGE

Inhibition of TH1 response

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32
Q

which cytokines are directly involved in allergic reactions?

A

IL-4 and 5

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33
Q

which cytokine is inovled in autoimmunity?

A

IL-17

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34
Q

what does immunosuppression mean?

A

a natural or artificial process which turns off the immune system either fully or partially. –> accidently or purposly

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35
Q

what can be the potential result of immunosuppression?

A

Immunodeficiency: the lack of effecient immune system that is susceptible to infection if the immune system is too switched off

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36
Q

what are the uses of immunosuppression?

A

transplant rejection
autoimmune disease
Lymphoproliferative diseases –> cancer of the immune system

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37
Q

what is the possible outcome if PRR doesn’t work early in life?

A

you are susceptible to pneumococcus early in life –~> no inflammatory response because the PRR is not working can lead to the development of meningitis but if you survive then adaptive immune system will kick in

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38
Q

what is a common problem when you lack the complement pathway?

A

If you don’t have complement pathway will get recurrent meningococcal

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39
Q

what does Hypersensitivity mean?

A

Undesirable, damaging, discomfort-producing and sometimes fatal reactions produced by the normal immune system (directed against innocuous antigens) in a pre-sensitized (immune) host.

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40
Q

what are the 4 types of hypersensitivity?

A

I - IgE MEDIATED REACTION
II - CYTOTOXIC REACTION
III - IMMUNE COMPLEX REACTION
IV - CELL MEDIATED REACTION (DTH)

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41
Q

give clinical features and common causes of type 1 hypersensivity?
Give example of allergic reactions

A

fast onset (15-30 min)
wheel and flare
can have a secondary reponse later on
common causes –> pollen, Bee venom and animal dander

Examples are: 
Hay fever 
Allergic asthma,
RHINITIS,
 DERMATITIS, 
FOOD ALLERGY
42
Q

which antibody is involved in type 1 hypersensitivity and what is the consequence of a severe attack?

A

IgE antibody

ANAPHYLAXIS

43
Q

what are the outcome to the body of type 1 hypersensitivity?

A

release of histamine
get Bronchospasm in smooth muscles
hypertension as blood vessel dilate and become leeky
mucous glands are affected –> coughing and production of mucous to try and get rid of the parasite

44
Q

how is immunoglobin E produced?

A

Produced by plasma cells from class-switched B cells under the control of IL-4 and CD40L - CD40 interaction

45
Q

What are the serum level of IgE and how well does it bind?

A

Low serum levels but high affinity to basophils and mast cells and forms stable binding over longer period.

46
Q

What occurs in the early phase reaction of type 1 hypersensitivty?

A

high-affinity IgE receptor at high density on the mast cell –> cross linkage occurs by allergn promotion which activated mast cells. This lead sto degranulation which release pre formed mediators and synthesis of lipid mediators.

47
Q

what are the pre mediators that are released during degranulation in type 1 hypersenisitivity?

A

Histamine –> stimulation of irritant nerve receptors, smooth muscle contraction and increase in vascular permeability
kallikrein –> activates bradykinin which has similar affects to histamine
TRYPTASE –> role unclear

48
Q

What cells are involved in late phase reaction of type 1 hypersensitivty?

A

Basophils –> similar to mast cells but work over longer period
Eosinophils –> contain granules of cytotoxic properties, attarcted to sight of infection by chemokines. Cause the release of granule content and damage to the tissue –> main cause of damage in allergic reaction

T cells are invovled both initial and late phase of the type 1. The active T cells produce cytokines that act as the driven activity for the main source of pathogensis in allergic reaction

49
Q

what is type 2 hypersensitivity?

A

antibody mediate cytotoxic response

50
Q

what happens in type 2 hypersensitivity?

A

Binding of the antibody to target antigen on the surface membrane causes:

activation of the complement cascade leading to cell lysis.
Aggregation of Fc portions of immunoglobulin/C3b with binding to FcRs/C3bR resulting in opsonisation, phagocytosis & destruction

51
Q

which antibody is the main antibody for the type 2 hypersensivity reaction?

A

IgM is the most effective as has 5 bits ( pentavelent)

but also complement binding IgG1 and 3 but need multiple binding sites

52
Q

what cells does type 2 hypersensivity occur in?

A

haematopoietic cells

53
Q

Give 4 examples of type 2 hypersnesitivity

A

ABO incompatability
Autoimmune haemolytic anaemias
Affecting neutrophils
Affecting platelets

54
Q

what drug can cause all 4 types of hypersensitivity?

A

Penicillin

55
Q

what occurs in type 3 hypersensitivity?

What antibody mediates this reaction

A
  1. IgG + Ag = AgAb complex this his deposits in parts of the body, if they accumulate in large enough quantities you get activation of the complement system
  2. FcR in complex bind C1q
  3. Complement activation leads to generation of activated complement fragments
    4a. C5a - attractant for neutrophils
    4b. C3b - Opsonin
  4. Attempted phagocytosis of complexes - release of enzymes, oxygen radicals
  5. Consequence is tissue damage

IgG mediated reaction

56
Q

what is type 4 hypersensitivity?

A

T cell mediated –> CD4 cells –> MHC class 2.

57
Q

What is granulomas?

What type of T cells are present and what do macrophages release?

A

Focal collections of inflammatory cells in tissues
Contain:
Macrophages
Epitheliod cells ( phagocytes that have engulfed foreign material)
Lymphocytes
Giant cells

T cells are TH1 type –> release IL-2 and IFN gamma
Macrophages release IL-12 critical in the initiation of the response

58
Q

Give example of mycobacterial infectious diseases that cause granulomas reactions

A

Tuberculosis
Atypical mycobacteria

Leprosy
Tuberculoid - Th1 - Protective
Lepromatous Th2 - Non-protective

59
Q

what is Osteomyelitis?

A

chronic condition of abcess in the bone marrow cavity. It is a bacterial infection most commonly involving Staphylococcus species. Comonly associated with complication of compound fractures

60
Q

what does Vascular endothelial growth factor (VEGF) do?

A

it is a vascular cell growth factor for endothelial cells–> increase vascular permeability and mitogenic for endothelial cells

61
Q

what Type of granulocyte takes part in allergic response?

A

EOSINOPHIL

62
Q

Cytokines recruit what cell type into sites of chronic inflammation?

A

lymphocytes

63
Q

what are giant cells associated with at sight of infection?

A

granulomas which is the formation of granuloma tissue in response to infection.

64
Q

what are langerhan cells?

A

Dendritic cells found in the skin epithelium

65
Q

what are the major components of the innate immune system?

A 
Pattern recognition receptor
Antimicrobial peptides
Complement components
Cytokines
Cells
66
Q

What is the common theme of recognition of PRR?

A

Recognition of:
Pathogen associated molecular patten
Or
Danger associated molecular pattern

67
Q

TNF is released from what cells 2, has what targets and thus what effects 4?

A

Released from Macrophages and T lymphocytes Targets and effects Endothelia - increased coagulation and inflammation Hepatocytes - increased acute phase proteins Neutrophils - increased activation Hypothalamus- increased fever

68
Q

IL6 is released from what cells 3, has what targets and what effects 2

A

Released from Macrophages and T lymphocytes and endothelia Targets and effects Hepatocytes - increased acute phase proteins B lymphocytes - increased proliferation

69
Q

what is the function of C3b in the complement pathway?

A

Opsonisation and removal of immune complexes

70
Q

What is the function of C3a and C5a in the complement pathway?

A

Phagocyte recruitment

71
Q

What makes lymphocytes unique and what occurs when there is a infection?

A

They each have a unique antigen receptor.

When there is a infection each lymphocyte rapidly replicates and the one that is specific to that infection will carry on proliferating

72
Q

What is the primary lymphoid organs?

A

Lymphocytes development and selection

B cells –> bone marrow
T cells –> thymus

73
Q

What is the secondary lymphoid organs?

A

Immune response

Spleen
Lymph nodes
Mucosal surface

74
Q

When are most of the T cells produced in your body and in what state are they?

A

Most of T cell are produced early in life so important you get exposure

They are niave until they encounter a antigen and then produce a immune response

75
Q

The range of antigen variability is estimated at what?

A

10 to power of 9

76
Q

What is VDJ recombonitation?

A

Recomboniation of different genes allow the creation of more B and T cells that are possible with just the normal number of genes.
Increase the variability of immune response

77
Q

What is the mechanism of antigen presenting cells?

A 
The antigen is internalised
The antigen is brocken down to peptides
THe peptide interacts with the newly synthesised class 2 molecule which will inturn be expressed on the surface
If it is foreign then this will activate T helper cells which in turn will produce cytokines to activate T killer cells, B cells etc
78
Q

When to T cells interact with antigens?

A

They interact with antigens when they are associated with MHC proteins

79
Q

What structure within cell will break down a bacteria?

A

Proteasome

80
Q

what type of immunity is B cells involved in?

A

They produce antibodies and are involved in humoral immunity

81
Q

What type of immunity are T killer cells involved in?

A

They are able to kill pathogens and are involved in cellular immunity

82
Q

What infections are patients with defeciency in PRR prone to?

A

Pneumoccocus and HSV

83
Q

What infection are patients with defeciency in macrophages and neutrophils prone to?

A

CGD, Staphylcoccus and Aspergillus

84
Q

What infection are patients with defeciency in complement proteins prone to?

A

meningococus

85
Q

What infection are patients with defeciency in B cells prone to?

A

Reccurent sino-pulmonary infection

86
Q

What infection are patients with defeciency in cytokines prone to?

A

Mycobacterium

87
Q

What infection are patients with defeciency in effector T cells prone to?

A

SCID and opportunistic infections

88
Q

How does sensitisation and the early phase reaction of a Type I hypersensitivity reaction work?

A

1) Exposed to an allergen 2) B cell has a receptor that recognises this allergen and presents allergen to CD4 cells 3) CD4 cells release IL 4 causing IgE Ab to be produced by plasma cells aswell as the formation of some memory cells 4) The IgE Ab binds to the IgE Fc receptor on the mast cell - cross linking the FcR1 (IgE receptor) The above process is sensitisation 5) On re-exposure to the same allergen, it binds to the IgE receptors on the now-sensitised mast cell inducing degranulation of pre-formed mediators and synthesis of lipid mediators leading to allergic response

89
Q

Degrenulation of mast cells in type 1 hypersensitivity acts on what structures?

A

1) Smooth muscle 2) Blood vessels 3) Mucous glands 4) Platelets 5) Sensory nerve endings 6) Eosinophils

90
Q

What is released by mast cell in the primary phase reaction?

A

Degranulation occurs and histamine and protease is released

91
Q

In the second phase/late response what is released by mast cell?

A

The arachanoid acid too:

Leukotrines: B4,C4 and D4
Postaglandin:D2

92
Q

what are the lipid mediators produced in the initial response of type 1?

A

Arachanoid acid derivatives

Via 5 lypoxgenase –> Leukotrines : LA4-LD4
Via Cyclo-oxygenase–> Prostaglandin: D2,E2,F2

93
Q

What disease is caused by immune complex depostion from type 3 reaction on the blood vessel walls?

A

Vasculitis

94
Q

What disease is caused because of immune complex depostion from type 3 reaction on the renal glomeruli?

A

Nephritis

95
Q

What disease is caused because of immune complex depostion from type 3 reaction on the joint space?

A

Arthritis

96
Q

What disease is caused because of immune complex depostion from type 3 reaction on the perivascular area?

A

Arthus reaction

97
Q

What disease is caused because of immune complex depostion from type 3 reaction on the capillary/bronchi intergace

A

Farmers lungs

98
Q

Inactivation is seen as the 5th hypersensitive reaction.

Give me 3 examples?

A

Direct e.g. to Intrinsic factor - B12 deficiency

Indirect : binding to e.g. hormone results in clearance of AgAb complex

Receptor blockade: e.g. To AChR in Myasthenia Gravis

99
Q

How does the tuberculin skin reaction work?

A

T cell mediated CD4 cells ( mhs class 2)

Small amount of mycobacterium tuberculosis is injected intradermally (Mantoux test)
In individuals with no immunity there is no effect
In individuals with previous exposure as a result of TB infection of BCG vaccine you get a local inflammatory response as T cells have already been sensitized
Langerhan’s cells present Ag to T cells which produce cytokines
Get infiltration of lymphocytes and macrophages around the small blood vessels and the activated macrophages cause tissue damage

100
Q

How does contact dermatitis work?

A

T cell-mediated cytotoxicity
CD8+ T cells (MHC Class I)

Small amounts of Ag (eg. nickel or poison ivy) bind to covalently to tissue or skin proteins - the sensitising agent is known as a hapten and the protein as a carrier
The hapten-carrier complex is presented as an Ag by Langerhan’s cells in conjunction with MHC II to CD4+ cells
Induction of T cells normally occurs after months of exposure to an Ag
Re-exposure to that Ag triggers the elicitation phase where effector T cells migrate to the epidermis to meet the Langerhans cells presenting the complex and release cytokines leading to skin inflammation

101
Q

What are diseases with unknown aetiology that cause granulomats reactions?

A

Sarcoidosis
Wegener’s Granulomatosis
Crohn’s disease

102
Q

What are langerhan cells?

A

They are dendrite cells on your skin and mucosa

EMS - MOD (5 decks)

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