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M- Pathology > 3 - Trowsdale > Flashcards

3 - Trowsdale Flashcards

1
Q

Adjuvant

A

Mixture, cue the immune system that an infection is taking place
Convert soluble protein into particulate matter
May contain bacterial products to stimulate macrophage and DCs
Eg complete freunds adjuvant (CFA) contains ground up mycobacterium

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2
Q

Central and peripheral tolerance

A

Central - occurs during lymphocyte development

Peripheral - after lymphocytes leave primary organs

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3
Q

Central tolerance
T cells
Selection

A

Positive - selecting T cells with some affinity for self
Negative - not selecting those that bind too strongly to self
Thymus

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4
Q

Central tolerance

B cells

A

Eliminated if react to abundant antigen in self cells as they develop

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5
Q

Peripheral tolerance

Why is a backup needed?

A

Many antigens are not expressed in the bone marrow or thymus

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6
Q

AIRE

A

Transcription factor
Turns on peripheral genes in thymus
Developing T cells may be exposed to their products

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7
Q

Peripheral tolerance

4

A

Ignorance
Split tolerance
Anergy
Suppression

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8
Q

Peripheral tolerance

Ignorance

A

Potentially self reactive T cells are not activated

-antigens in immunologically privileged sites eg brain eye and testis

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9
Q

Peripheral tolerance

Split tolerance

A

Auto reactive B cells, but no T cell help

It takes more antigen to tile rise B cells than it does T cells

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10
Q

Peripheral tolerance

Anergy

A

Non responsiveness
T cell receptor engaged but second signal absent
Biochemical changes to anergised cell so it no longer responds

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11
Q

Peripheral tolerance

Suppression

A

Treg (regulatory Cd4 cell) from thymus
Cd25+ (IL2 receptor +ve)
Express fox3p transcription factor
Removal of Cd25 results in attack if self tissue

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12
Q

How do Tregs act

A

On contacting self antigen presented by MHC2, they suppress the proliferation of naive T cells
Non inflammatory cytokines IL4, IL10 and TGFB contribute to down modulation

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13
Q

Medawars neonatal tolerance experiment

A

Nice of strain A injected at birth with bone marrow from strain B
Grafted with skin from strain B
Accepted, when normally wouldn’t

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14
Q

How do bone marrow cells from mouse B establish chimerism in the host?

A

Differentiate into APCs
Migrate to thymus
Tolerise developing thymocytes

Lifelong chimerism - transfer must be at birth when there are insufficient T cells to destroy the donor stem cells

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15
Q

What causes lack of immune response of mother to fetus?

A
  • Physical barrier to mothers T cells
  • Lack of MHC1 expression. Trophoblast cells do not express MHC1 so are not targets
  • Production of immunosuppressive factors such as a-fetal protein
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16
Q

Inhalation tolerance

A

MHC binding peptides are aerosolised via nostril

Animal rendered tolerant to that peotide

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17
Q

Co receptor blockade

A

Monoclonal antibodies to coreceptors CD4/8, B7, CD40

Development of tolerance

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18
Q

How do microbes evade the immune system?

A
  • fungal spores coated in hydrophobin, immunologically inert

- vary surface antigens, different strains with different capsular polysaccharides

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19
Q

Antigenic drift

A

Change surface proteins by mutation

Eg flu

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20
Q

Antigenic shift

A

Change surface proteins by recombination with bird or pic viruses

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21
Q

Original antigenic sin

A

Individual only makes antibody against epitopes from original virus, when reinfected with mutated virus

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22
Q

Hashimoto’s thyroiditis

Graves’ disease

A

Autoimmune disease against thyroid

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23
Q

Pernicious anaemia

A

Autoimmune disease against stomach

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24
Q

Why organ specific autoimmunity?

A

Well vascularised

Make organ specific proteins

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25
Q

Non organ specific autoimmune targets

A

Skin (scleroderma)
Kidney (systemic lupus erythematosis)
Joints (rheumatoid arthritis)

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26
Q

Autoimmunity

Direct antibody mediated effects

A

Similar to type 2 hypersensitivity
Autoantibodies bind receptor
Can cause overproduction of hormone (graves) or block binding (myasthenia gravis)

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27
Q

Graves’ disease

A

Auto antibodies on TSH receptor

Unregulated overproduction of thyroid hormones

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28
Q

Myasthenia gravis

A

Autoantibodies to ACh receptor
Diminish neuromuscular transmission
Block binding and cause down regulation if receptor

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29
Q

Rheumatic fever

A

Direct tissue pathology following antibody bunding

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30
Q

Autoimmunity

Immune complex mediated effects

A

Similar to type 3 hypersensitivity

SLE, vasculitis

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31
Q

Systemic lupus erythematosis

A

Immune complex mediated
Autoantibodies
Butterfly rash on face
Depletion of complement

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32
Q

Autoimmunity

T cell mediated effects

A 
Similar to type 4 hypersensitivity
T1D
RA
MS
Tissue destruction without auto antibody 
-cytotoxicity by T cells
-destruction by TNF
-macrophages and bystander killing
-apoptosis by fas ligand
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33
Q

CFA

A

Complete freunds adjuvant

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34
Q

Haemolytic anaemia

  • Auto antigen
  • Consequence
A

Rh blood group antigens

Destroy RBC

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35
Q

Good pastures syndrome

  • Auto antigen
  • Consequence
A

Collagen type 4

Glomerulonephritis

36
Q

Graves’ disease

  • Auto antigen
  • Consequence
A

TSH receptor

Hyperthyroidism

37
Q

Myasthenia gravis

  • Auto antigen
  • Consequence
A

ACh receptor

Progressive weakness

38
Q

Subacute bacterial endocarditis

  • Auto antigen
  • Consequence
A

Bacterial antigen

Glomerulonephritis

39
Q

Systemic lupus erythematosis (SLE)

  • Auto antigen
  • Consequence
A

DNA, histones, ribosomes

Glomerulonephritis, vasculitis, arthritis

40
Q

Type 1 diabetes

  • Auto antigen
  • Consequence
A

Pancreatic cell antigen

B cell destruction

41
Q

Rheumatoid arthritis

  • Auto antigen
  • Consequence
A

Synovial joint antigens

Joint inflammation and destruction

42
Q

Multiple sclerosis

  • Auto antigen
  • Consequence
A

Myelin basic protein proteolipoprotein

Brain degeneration, paralysis

43
Q

Generic predisposition

Autoimmune disease associated with

A

HLA allotypes

44
Q

Autoimmune sympathetic opthalmia

A

Damage to one eye leads to autoimmune attack of contra lateral wye

45
Q

Autoimmunity - T cell bypass

Tolerance being bypassed

A

Modification - generates neoantigen recognised by T cells
Inflammation - pAPCs, activate ignorant auto reactive T cells
Molecular mimicry - antibodies cross react with self antigens

46
Q

Treatment of autoimmune disease

A

Organ specific - agents exert metabolic control (thyroxine)

Immunosuppressive drugs

47
Q

Cd4 cells

TH1

A

Produce cytokines
Activate macrophages
Destroy intracellular microbes

48
Q

Cd4 cells

TH2

A

Produce cytokines
Promote Humoral response
Stimulate eosinophils and mast cells

49
Q

Cd4 cells

TH17

A

Anti microbial immunity at epithelial barriers

Recruit neutrophils

50
Q

Cd4 cells

Tfh

A

T follicular helper cells
In B cell follicles
Activate b cells

51
Q

Cd4 cells

Treg

A

Suppress T cell activity

52
Q

Hypersensitivity

A

Over reactive, damaging, immunesystem

53
Q

Type 1 hypersensitivity

A

Allergic reaction
Host has pre existing IgE antibody
Mast cells activated by cross linking of FceRI receptors, via antigen binding to bound IgE
IgE is pre bound to receptor an is cross linked by antigen

54
Q

Common allergens

A 
Pollens
Food
Drugs
Insect products
Animal hait
55
Q

Properties of allergens

A

Low mw
Highly soluble, diffuse into mucus
Peptides bind MHC class 2
Favour IL4 producing, Th2 response

56
Q

Skin price test, what is wheal and flare?

A

Wheal - edema

Flare - erythema (increased blood flow)

57
Q

Atopic individuals

A

Genetically predisposed to allergies
Higher IgE levels
Protection against parasites
Make IgE instead of IgG

58
Q

Systemic anaphylaxis

A

Increased permeability of blood vessels
Extreme drop in blood pressure
Anaphylactic shock

59
Q

Type 2 hypersensitivity

A

IgM or IgG binding to cells or tissue antigens

Triggers clearance of the cell by tissue macrophages in the spleen (Fcgamma) or complement lysis

60
Q

Examples of type 2 hypersensitivity

A

Hemolytic anemia

Thrombocytopenia (destruction of platelets)

61
Q

ABO blood group is the only…

A

Histocompatability antigen for which pre-existing antibody is present in naive recipients

62
Q

ABO blood grouping

Molecules consist of…

A 
Core H antigen
O - unmodified
A - adds a terminal N-acetylgalactosamine
B - adds a terminal galactose
AB - adds both modifications
63
Q

Haemolytic disease of the newborn

HDNB

A

Mother rhesus negative
Child rhesus positive
Rh+ into maternal circulation at birth
IgG cross placenta and affect subsequent Rh+ baby
Give anti-Rh antibody before mother reacts

64
Q

Type 3 hypersensitivity

A 
Inability to clear immune complexes 
IgG, complexes bind to FcgammaRIII
Soluble antigen in high quantities
Immune complexes deposited in tissue
Mast cell and complement cause local tissue damage
65
Q

Examples of type 3 hypersensitivity

A 
Post infection complications
Arthritis
Glomerulonephritis
Pigeon fanciers/farmers lung-fungal spores
Systemic lupus
66
Q

Arthus reaction

A

Local type 3 hypersensitivity reaction
Triggered in skin of sensitised individuals
Broad hard lump

67
Q

Type 4 hypersensitivity

A 
Delayed type
Mediated by T cells
Effect maximal in 48-72hrs
TB
Damage through Th1 cells activating macrophages and cytokines
68
Q

Examples of type 4 hypersensitivity

A

Th1 mediated
Granulomas
Tuberculosis
Poison ivy

69
Q

What is the problem with transplanting tissue?

A

Variation in polymorphic surface antigens encoded by the MHC
And other minor antigens

70
Q

Autologous transplantation

A

Same species

71
Q

Syngeneic transplantation

A

Same genetic makeup

Identical twins

72
Q

Xenogeneic transplantation

A

Different species

73
Q

Allogenic transplants

A

Display immunological memory
Primed by allograft
When regrafted, it is rejected more rapidly
Second set rejection is caused by a memory immune response

74
Q

Transplantation

Direct recognition

A

Of donor MHC

75
Q

Transplantation

Indirect recognition

A

Of an antigen presented by self MHC molecules

76
Q

Hyper acute rejection

A

Rapid
Pre existing antibody
Damage by complement activation and aggregation of platelets that block microvasculature

77
Q

DAF

A

Decay accelerating factor

Disables complement on self tissue

78
Q

Acute graft recognition

A

T cell recognition

Not an issue in blood transfusions as RBCs do not carry MHC antigens

79
Q

Acute graft rejection

Direct recognition of allo MHC

A

Naive individuals have a high frequency of T cell receptors reactive with allo-MHC products
Activated at low affinity
Alloreactive T cells carried back to graph from lymph node and attack directly

80
Q

Acute graft rejection

Indirect recognition

A

Uptake of allogeneic proteins by APCs and presentation to T cells by self MHC molecules
MHC sharing increases reactivity

81
Q

Chronic rejection

A

Years after transplant

Immune response against blood vessel

82
Q

Transplant

Privileged sites

A

Cornea
No lymphatic drainage
Lack vascularisation

83
Q

Transplant

Vascularised solid organs

A

Kidney, lung, liver, heart, pancreas

84
Q

Transplant

Haemopoietic stem cell

A

Peripheral blood
Bone marrow
Cord blood
Graft may reject host

85
Q

How many MHC antigen polymorphic genes

A

6

86
Q

Immunosuppressant drugs for transplantation

A

Steroids - systemic immunosuppressive effects
Cytotoxic drugs - cell death, on entry to cell cycle
Immunosuppressive - target cell signalling pathway in lymphocytes

M- Pathology (7 decks)

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