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4TH YEAR - CSIM2 > Immunology > Flashcards

Immunology Flashcards

1
Q

What is the role of the macrophage:

a) at rest?
b) when primed?

A

a) Processes cellular debris

b) Phagocytosis of invading microorganisms (hyper activation)
Presentation of antigen at the lymph node

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2
Q

What happens when the macrophage is ‘primed’ in response to IFNgamma?

A

It expresses more MHCII so that it can become an antigen presenting cell

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3
Q

What is ‘hyper activation’?

A

Component of the innate response:

  • Toll like receptor recognises PAMP on pathogen
  • Macrophage has increased numbers of reactive oxygen molecules and lysosomes
  • Macrophages ingest and kill pathogens (phagocytosis)
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4
Q

What chemicals does the activated macrophage release?

A 
IL1B
TNFa
IL6
CXCL8
IL12
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5
Q

What does IL1B do?

A

Local - activates vascular endothelium and lymphocytes

Systemic - fever, activates IL-6 production

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6
Q

What does TNFa do?

A

Local - activates vascular endothelium and increases its permeability so that more IgG, complement and cells go into the tissue and more fluid is drained to the lymph nodes
Systemic - fever, shock

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7
Q

What does IL-6 do?

A

Local - activates lymphocytes and increases antibody production by plasma cells
Systemic - fever, acute phase protein production

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8
Q

What does CXCL8 do?

A

Local - recruits neutrophils, basophils and T cells to the site of infection

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9
Q

What does IL12 do?

A

Activates NK cells and induces CD4 T cells to become Th1 cells

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10
Q

How does a natural killer cell work?

A
  1. Recognises infected cells in the absence of antibodies or MHC molecules
  2. Forms a pore in the cell membrane of the target cell so that granzymes can enter and induce apoptosis
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11
Q

How does a neutrophil work?

A

Ingests and kills microbes by phagocytosis, hallmark of acute inflammation

THEY ARE NOT APCs

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12
Q

What chemokines often attract immune cells to the site of infection?

A

IFNgamma, IL8

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13
Q

What is the role of dendritic cells?

A

At rest - sample the environment
Primed - Phagocytosis of pathogens and APC, travels to local lymph node to await T cell sampling and then activation. Also secretes monocytes to the site of infection

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14
Q

How long do dendritic cells live?

A

They die after 1 week at the LN, to prevent T cell activation in absence of infection

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15
Q

What do dendritic cells make when there is no infection, and what is the purpose of this?

A

TGFb and IL6 (in v small amounts)

This activates CD4T cells to express FOXP3 and become Tregs

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16
Q

What do dendritic cells produce when there is an infection?

A

IL6, IL12, IL4

These chemicals cause naive CD4 t cells to become T helper cells

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17
Q

What are the different types of B cells and what do they do?

A

Plasma cells - antibody production
Memory cells - enable faster antibody production in future infections
Follicular cells - reside in the lymph nodes

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18
Q

What is the role of a B cell in the early stage of an infection?

A

They can act as a APC as they have a very high affinity for the antigen

They need to be activated by an activated T cell

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19
Q

What happens once a B cell has been activated?

A

a) form a primary focus in nearby medullary cords

a) forms a germinal centre in a nearby follicle

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20
Q

What is the purpose of a germinal centre?

A

Some cells will leave the primary focus to form a germinal centre.

It is a site where mature B cells:

  • differentiate
  • proliferate
  • mutate their antibody genes (somatic mutation)
  • class switch their antibodies (Igm - Igg)

At the end of this process, B cells will leave as a memory cell, plasma cell, or they may have to restart the process again

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21
Q

What are the different types of T cells and what do they do?

A

CD4 T helper - assist in B cell maturation and activation of cytotoxic T cells and B cells and macrophages

CD8 T killer - destroy virus infected cells

T regulatory (FOXP3) - shut down T cell mediated immunity towards the end of a reaction and prevent autoimmunity

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22
Q

What activates CD4 T helper cells?

A

MHCII molecules on APCs

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23
Q

What activates CD8 T killer cells?

A
  • MHCI molecules on all nucleated cells

- Activation by CD40L from cytokine secretion by the CD4 cell

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24
Q

What are the three APCs?

A

Dendritic cells
Macrophages
B cells

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25
Q

Describe the two pathways that stop the immune system

A

Intrinsic - lack of survival sign prompts release of cytochrome c from the mitochondria causing apoptosis

Extrinsic - Fas causes activation of death domains with FADD

Both pathways involve recruitment of PROCASPASE, which induces APOPTOSIS

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26
Q

What is an immune privileged site?

A

Somewhere where there are no immune cells eg. eyes, brain, testes

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27
Q

What is the definition of auto reactivity?

A

The presence of immune response reactive with self antigens, which is often harmless

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28
Q

What is autoimmunity?

A

A disease process resulting from auto reactivity

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29
Q

What is central tolerance?

A
  • In the thymus and bone marrow, maturing lymphocytes are exposed to self-antigens from MHCII molecules
  • Lymphocytes that bind strongly to self-antigen are deleted by apoptosis
  • Those that are weakly auto reactive may become Tregs, which go on to regulate peripheral tolerance

This process is known as negative selection

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30
Q

What is peripheral tolerance?

A
  • Tregs, DCs and other regulatory cells recognise self-reactive T/B cells in the periphery
  • These cells are either inactivated or deleted
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31
Q

What is a type I hypersensitivity reaction?

A

An IgE mediated response in which:

  • Antigen induces cross linking of IgE bound to mast cells and basophils
  • When antigen is reintroduces, vasoreactive markers are released from degranulation of the mast cell
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32
Q

What is an example of a type 1 reaction?

A

Anaphylaxis

Allergy

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33
Q

What is a type 2 hypersensitivity reaction?

A

An IgM/IgG/complement mediated response in which:

  • There is a cytotoxic reaction against a harmless antigen
  • Antibody-mediated
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34
Q

What in an example of a type 2 reaction?

A

Blood transfusion reaction
Myasthenia Gravis
Graves Disease
Goodpastures

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35
Q

What is a type 3 hypersensitivity reaction?

A

An IgM/IgG/Neutrophil mediated reaction in which:

- An immune complex is formed, which is deposited in various tissues causing massive neutrophil infiltration

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36
Q

What is an example of a type 3 reaction?

A

Vasculitis
Rheumatoid arthritis
SLE

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37
Q

What is a type 4 hypersensitivity reaction?

A

A T cell mediated reaction in which:

  • Sensitised TH1 cells release cytokines that activate macrophages or T cells
  • This is a DELAYED reaction
38
Q

What is an example of a type 4 reaction?

A

SJS
Chronic transplant rejection
Contact dermatitis

39
Q

What are the 3 phases of an IgE mediated allergy?

A
  1. Sensitisation
  2. Immediate
  3. Late phase
40
Q

Describe sensitisation in an IgE reaction?

A
  • Allergen recognised and presented by APC
  • T cell recognises it and becomes malicious TH2 cell
  • This induces the B cell to produce IgE (instead of IgM)
  • IgE connects to the mast cell
41
Q

Describe the immediate reaction in an IgE response?

A
  • Allergen attaches to IgE
  • Mast cell and basophil crosslink releasing histamine
  • Bronchoconstriction, vasodilation, peristalsis and nerve stimulation
42
Q

Describe the late phase of an IgE response?

A
  • Despite allergen having left the body, the response is prolonged by ILs and leukotrienes
  • Recruitment of other immune cells to exaggerate the response
  • Takes 2-24hr after exposure
43
Q

How can an allergy be investigated?

A
  • Skin prick test
  • RAST (blood test looking for IgE)
  • Intradermal testing
  • Patch testing
  • Oral challenge
44
Q

How can an allergy be treated?

A
  1. Remove trigger
  2. Histamine blocker
  3. Mast cell stabiliser
  4. Prednisolone
  5. Montelukast
  6. Immunotherapy
  7. Olantuzimab
45
Q

What are the signs of anaphylaxis?

A
  • Skin flushing
  • Hives
  • Difficulty swallowing or speaking
  • Vomiting
  • Hoarse voice
  • Collapse
46
Q

How is anaphylaxis managed?1

A
  1. Adrenaline 0.5ml of 1in1000 IM
  2. Fluid bolus stat
  3. Chlorphenamine IV
  4. Hydrocortisone IV
47
Q

Why is autoimmunity difficult to clear?

A

Destruction of self-antigen leads to release of more self-antigen

48
Q

Describe 4 type II autoimmune reactions, and their antigens

A

Goodpastures syndrome (type IV collagen)

Myasthenia Gravis (ACh receptor)

Haemolytic anaemia of the newborn (RBC)

Graves disease (TSH receptor)

49
Q

Describe 3 type III autoimmune reactions and their antigens

A

SLE (nuclear antigen)

Rheumatoid arthritis (citrullinated protein)

Farmers lung (inhaled antigens)

50
Q

Describe 3 type IV autoimmune reactions and their antigens

A

Hashimotos thyroiditis (thyroglobulin)

Type 1 diabetes (pancreatic b cell proteins)

MS (myelin)

51
Q

What happens in Goodpastures disease?

A

Autantibodies form against type IV collagen in the alveoli and glomerular basement membranes, causing renal and respiratory symptoms

52
Q

How is good pastures diagnosed?

A

Anti-GBM antibodies

Kidney biopsy

53
Q

What happens in SLE?

A

Antibodies form against nuclear and cytoplasmic antigens, reflecting a GLOBAL loss of self tolerance

54
Q

What are the symptoms of SLE?

A 
Malar, photosensitive rash
Glomerulnophritis
Raynauds
Pleurisy
Oral ulcer
Neurological
Cardiological 
Anaemia
Arthritis
55
Q

How is SLE diagnosed?

A

ANA antibodies, IgG, dsDNA and ESR are all raised

Low levels of complement

56
Q

Name four primary antibody immunodeficiencies

A

X linked agammglobulinaemia
AR agammaglobulinaemia
Common variable immunodeficiency
Transient hypogammaglobulinaemia of infancy

In all of these disease, one or more isotopes are decreased or non-functioning

57
Q

What could cause secondary antibody immunodeficiency?

A

Protein losing states

Rituximab

58
Q

What are the 3 types of primary neutrophil deficiency?

A
  1. Neutropenia - inability to produce neutrophils
  2. Failure of migration - may function but can’t reach site of action
  3. Failure of function
59
Q

Mutations in which genes can cause primary neutropenia?

A

HAX1
ELA2
WAS

60
Q

What is leukocyte adhesion deficiency?

A

A primary neutrophil deficiency involving failure of migration of leucocytes, causing frequent bacterial infection

61
Q

What is chronic granulomatous disease?

A

A primary neutrophil deficiency in which immune cells can’t form reactive oxygen species so can’t function

62
Q

What could cause secondary neutrophil immunodeficiency?

A

Bone marrow failure
Certain drugs
Chemo/radiotherapy

63
Q

What is a primary complement deficiency?

A

Any deficiency of a complement factor, most produced in the liver, that results in recurrent specific infection (often streptococci or Hib)

64
Q

What would C5-9 deficiency cause?

A

Recurrent meningococcal infection

65
Q

Give 4 examples of primary T cell deficiencies

A

SCID (b cells also deficient)
Wiskott Aldrich
CD40L deficiency
Di George

66
Q

What could cause secondary T cell deficiency?

A

Drugs (biologics/monoclonal abs)
Chemo/radio
HIV infection

67
Q

Give an example of a specific molecular deficiency?

A

IL-12/IFNgamma deficiency - these usually protect against mycobacteria

TLR3/UNC/TRAF deficiency - these usually protect against herpes

These may not be picked up unless the patient is exposed to the certain pathogen

68
Q

What is AIRE deficiency?

aka APS-1/APECED

A

Dysfunction of multiple endocrine glands due to a defect in the autoimmune regulator, which is involved in CENTRAL TOLERANCE

69
Q

What are the symptoms of AIRE deficiency?

A 
Hypoparathyoridism
Hypogonadism
Vitiligo
Alopecia
Malabsorption
Candidiases
Cataract
70
Q

What is IPEX syndrome?

A

A lack of PERIPHERAL TOLERANCE, due to a mutation in the gene that makes FOXP3, resulting in a dysfunctional Tregs

71
Q

What are the symptoms of IPEX syndrome?

A 
Severe diarrhoea
Psoriasis
Eczema
Nail dystrophy
Endocrinopathies
Hypothyroidism
72
Q

What is autoimmune lymphoproliferative syndrome?

A

A disease of immune dysregulation in which there is abnormal survival of lymphocytes due to defective Fas mediated apoptosis (extrinsic pathway)

73
Q

What are the symptoms of autoimmune lymphoproliferative syndrome?

A

Lymphadenopathy
Hepatosplenomegaly
Risk of lymphoma

74
Q

What is haemophagocytic lymphohistiocytosis?

A

A disease of immune dysregulation in which there is severe hyper inflammation due to proliferation of lymphocytes that secrete high amounts of cytokine (CYTOKINE STORM)

Presents with fever, splenomegaly

75
Q

What is HUS?

A 
Can be caused by mutations in complement activation (factor H/I/MCP), or just bacterial/viral infection.
Triad of:
- Haemolytic anaemia
- AKI
- Thrombocytopenia
76
Q

What is pulmonary alveolar proteinosis?

A

Mutation in GM-CSF phagocyte, causing build up of surfactant aggregates, and non infectious respiratory failure

77
Q

What are the 3 forms of transplant rejection?

A
  1. Hyperacute - minutes
  2. Acute - days/weeks
  3. Chronic - months/years
78
Q

What happens in hyper acute transplant rejection ?

A

Recipient carries pre-existing ALLOANTIBODIES against BLOOD GROUP ANTIGENS or NON-SELF MHC, which react with donor antigen

This initiates the complement and coagulation cascade so the organ vessel becomes blocked and dies

79
Q

What happens in acute rejection?

A

Recipient mounts a cell-mediated or humoral response against foreign tissue, causing cell death in the organ.

This always happens, which is why you need immunosuppresion

80
Q

What happens in chronic rejection? What causes it?

A

Involves a combination of type 3 and type 4 hypersensitivity reactions (immune complex, complement and T cells), mimicking a chronic inflammatory disease ie. involving FIBROSIS. This is irreversible.

Caused by -

  • Chronic allograft vasculopathy
  • Viral infection
  • Ischaemia-reperfusion injury
81
Q

Describe direct alloantigen presentation

A

Foreign peptide presents with its own foreign MHC

This donor APC activates recipient T cells causing attack

THIS IS ACUTE REJECTION

82
Q

Describe indirect alloantigen presentation

A

Recipient APC presents foreign peptide with self MHC to the recipient lymph node.

This activated T cells (although fewer than in direct) causing attack.

THIS IS CHRONIC REJECTION

83
Q

Which forms of alloantigen presentation are present in:

a) acute rejection
b) chronic rejection

A

a) direct

b) indirect

84
Q

How can healthcare professionals prevent rejection?

A
  1. Blood group matching
  2. HLA matching.
  3. Immunosuppresion
85
Q

What is Graft vs Host disease?

A

This is when graft bone marrow or stem cells mount an immune response against the host and the body is unable to mount a response against this due to immunosuppression.

86
Q

What are the risk factors for GVHD?

A
  1. Transfusion of unirradiated blood products
  2. Solid organ transplant (particularly liver)
  3. Allogenic haemoatopoietic cell transplantation (used for blood cancers)
87
Q

What are the symptoms of GVHD?

A

Diarrhoea, rash, jaundice, liver dysfunction

Can affect any body system,

88
Q

How can GVHD be prevented?

A
  • Same sex, young, low parity donor

- Immunosuppress with cyclosporin, steroids and mycophenolate

89
Q

What is an HSC transplant?

A

Treatment for certain blood-marrow precursor cells (leukemia/lymphoma)

Recipient bone marrow must be treated with aggressive chemo/radio prior to replacement

90
Q

What is GvLE? What is the disadvantage>

A

Graft vs leukaemia effect

This is a method of preventing GVHD:

  • Irradiate donor HSC in vitro to remove allogenic T cells
  • Any T cells that develop in vivo will not react to host cells

However this causes an increased risk of leukaemic recurrence.

4TH YEAR - CSIM2 (20 decks)

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