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4TH YEAR - CSIM2 > Immunology > Flashcards

Immunology Flashcards

(90 cards)

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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
Describe the two pathways that stop the immune system
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
26
What is an immune privileged site?
Somewhere where there are no immune cells eg. eyes, brain, testes
27
What is the definition of auto reactivity?
The presence of immune response reactive with self antigens, which is often harmless
28
What is autoimmunity?
A disease process resulting from auto reactivity
29
What is central tolerance?
- 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
30
What is peripheral tolerance?
- Tregs, DCs and other regulatory cells recognise self-reactive T/B cells in the periphery - These cells are either inactivated or deleted
31
What is a type I hypersensitivity reaction?
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
32
What is an example of a type 1 reaction?
Anaphylaxis | Allergy
33
What is a type 2 hypersensitivity reaction?
An IgM/IgG/complement mediated response in which: - There is a cytotoxic reaction against a harmless antigen - Antibody-mediated
34
What in an example of a type 2 reaction?
Blood transfusion reaction Myasthenia Gravis Graves Disease Goodpastures
35
What is a type 3 hypersensitivity reaction?
An IgM/IgG/Neutrophil mediated reaction in which: | - An immune complex is formed, which is deposited in various tissues causing massive neutrophil infiltration
36
What is an example of a type 3 reaction?
Vasculitis Rheumatoid arthritis SLE
37
What is a type 4 hypersensitivity reaction?
A T cell mediated reaction in which: - Sensitised TH1 cells release cytokines that activate macrophages or T cells - This is a DELAYED reaction
38
What is an example of a type 4 reaction?
SJS Chronic transplant rejection Contact dermatitis
39
What are the 3 phases of an IgE mediated allergy?
1. Sensitisation 2. Immediate 3. Late phase
40
Describe sensitisation in an IgE reaction?
- 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
Describe the immediate reaction in an IgE response?
- Allergen attaches to IgE - Mast cell and basophil crosslink releasing histamine - Bronchoconstriction, vasodilation, peristalsis and nerve stimulation
42
Describe the late phase of an IgE response?
- 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
How can an allergy be investigated?
- Skin prick test - RAST (blood test looking for IgE) - Intradermal testing - Patch testing - Oral challenge
44
How can an allergy be treated?
1. Remove trigger 2. Histamine blocker 3. Mast cell stabiliser 4. Prednisolone 5. Montelukast 6. Immunotherapy 7. Olantuzimab
45
What are the signs of anaphylaxis?
- Skin flushing - Hives - Difficulty swallowing or speaking - Vomiting - Hoarse voice - Collapse
46
How is anaphylaxis managed?1
1. Adrenaline 0.5ml of 1in1000 IM 2. Fluid bolus stat 3. Chlorphenamine IV 4. Hydrocortisone IV
47
Why is autoimmunity difficult to clear?
Destruction of self-antigen leads to release of more self-antigen
48
Describe 4 type II autoimmune reactions, and their antigens
Goodpastures syndrome (type IV collagen) Myasthenia Gravis (ACh receptor) Haemolytic anaemia of the newborn (RBC) Graves disease (TSH receptor)
49
Describe 3 type III autoimmune reactions and their antigens
SLE (nuclear antigen) Rheumatoid arthritis (citrullinated protein) Farmers lung (inhaled antigens)
50
Describe 3 type IV autoimmune reactions and their antigens
Hashimotos thyroiditis (thyroglobulin) Type 1 diabetes (pancreatic b cell proteins) MS (myelin)
51
What happens in Goodpastures disease?
Autantibodies form against type IV collagen in the alveoli and glomerular basement membranes, causing renal and respiratory symptoms
52
How is good pastures diagnosed?
Anti-GBM antibodies | Kidney biopsy
53
What happens in SLE?
Antibodies form against nuclear and cytoplasmic antigens, reflecting a GLOBAL loss of self tolerance
54
What are the symptoms of SLE?
``` Malar, photosensitive rash Glomerulnophritis Raynauds Pleurisy Oral ulcer Neurological Cardiological Anaemia Arthritis ```
55
How is SLE diagnosed?
ANA antibodies, IgG, dsDNA and ESR are all raised Low levels of complement
56
Name four primary antibody immunodeficiencies
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
What could cause secondary antibody immunodeficiency?
Protein losing states | Rituximab
58
What are the 3 types of primary neutrophil deficiency?
1. Neutropenia - inability to produce neutrophils 2. Failure of migration - may function but can't reach site of action 3. Failure of function
59
Mutations in which genes can cause primary neutropenia?
HAX1 ELA2 WAS
60
What is leukocyte adhesion deficiency?
A primary neutrophil deficiency involving failure of migration of leucocytes, causing frequent bacterial infection
61
What is chronic granulomatous disease?
A primary neutrophil deficiency in which immune cells can't form reactive oxygen species so can't function
62
What could cause secondary neutrophil immunodeficiency?
Bone marrow failure Certain drugs Chemo/radiotherapy
63
What is a primary complement deficiency?
Any deficiency of a complement factor, most produced in the liver, that results in recurrent specific infection (often streptococci or Hib)
64
What would C5-9 deficiency cause?
Recurrent meningococcal infection
65
Give 4 examples of primary T cell deficiencies
SCID (b cells also deficient) Wiskott Aldrich CD40L deficiency Di George
66
What could cause secondary T cell deficiency?
Drugs (biologics/monoclonal abs) Chemo/radio HIV infection
67
Give an example of a specific molecular deficiency?
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
What is AIRE deficiency? | aka APS-1/APECED
Dysfunction of multiple endocrine glands due to a defect in the autoimmune regulator, which is involved in CENTRAL TOLERANCE
69
What are the symptoms of AIRE deficiency?
``` Hypoparathyoridism Hypogonadism Vitiligo Alopecia Malabsorption Candidiases Cataract ```
70
What is IPEX syndrome?
A lack of PERIPHERAL TOLERANCE, due to a mutation in the gene that makes FOXP3, resulting in a dysfunctional Tregs
71
What are the symptoms of IPEX syndrome?
``` Severe diarrhoea Psoriasis Eczema Nail dystrophy Endocrinopathies Hypothyroidism ```
72
What is autoimmune lymphoproliferative syndrome?
A disease of immune dysregulation in which there is abnormal survival of lymphocytes due to defective Fas mediated apoptosis (extrinsic pathway)
73
What are the symptoms of autoimmune lymphoproliferative syndrome?
Lymphadenopathy Hepatosplenomegaly Risk of lymphoma
74
What is haemophagocytic lymphohistiocytosis?
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
What is HUS?
``` Can be caused by mutations in complement activation (factor H/I/MCP), or just bacterial/viral infection. Triad of: - Haemolytic anaemia - AKI - Thrombocytopenia ```
76
What is pulmonary alveolar proteinosis?
Mutation in GM-CSF phagocyte, causing build up of surfactant aggregates, and non infectious respiratory failure
77
What are the 3 forms of transplant rejection?
1. Hyperacute - minutes 2. Acute - days/weeks 3. Chronic - months/years
78
What happens in hyper acute transplant rejection ?
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
What happens in acute rejection?
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
What happens in chronic rejection? What causes it?
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
Describe direct alloantigen presentation
Foreign peptide presents with its own foreign MHC This donor APC activates recipient T cells causing attack THIS IS ACUTE REJECTION
82
Describe indirect alloantigen presentation
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
Which forms of alloantigen presentation are present in: a) acute rejection b) chronic rejection
a) direct | b) indirect
84
How can healthcare professionals prevent rejection?
1. Blood group matching 2. HLA matching. 3. Immunosuppresion
85
What is Graft vs Host disease?
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
What are the risk factors for GVHD?
1. Transfusion of unirradiated blood products 2. Solid organ transplant (particularly liver) 3. Allogenic haemoatopoietic cell transplantation (used for blood cancers)
87
What are the symptoms of GVHD?
Diarrhoea, rash, jaundice, liver dysfunction Can affect any body system,
88
How can GVHD be prevented?
- Same sex, young, low parity donor | - Immunosuppress with cyclosporin, steroids and mycophenolate
89
What is an HSC transplant?
Treatment for certain blood-marrow precursor cells (leukemia/lymphoma) Recipient bone marrow must be treated with aggressive chemo/radio prior to replacement
90
What is GvLE? What is the disadvantage>
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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