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Clinical Immunology > Book > Flashcards

Book Flashcards

1
Q

Define the difference between class I and class II MHC molecules

A 
Class I presents protein fragments to killer T cells whereas class II presents peptides to helper T cells 
Class I are expressed on almost every kind of cell whereas class II are expressed exclusively on cells of the immune system
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2
Q

What can trigger a dendritic cell to activate?

A

When neutrophils and macrophages release tumour necrosis factor (TNF) when destroying an attacker
Interferon alpha and beta released by virus-infected cells
Pattern-recognition receptors on dendritic cells (e.g. TLR)

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3
Q

Why is a short lifetime of a dendritic cell a good thing?

A

The shorter the lifespan encourages a proportionate response to the severity of the attack

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4
Q

What do mature dendritic cells activate?

A
  • Naïve T cells

* Activated tissue macrophages

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5
Q

Why do activated tissue macrophages need activating?

A
  • To re-stimulate experienced T cells

* If they are not re-stimulated, they will “rest” thinking the battle is over

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6
Q

What molecules are involved in antigen recognition on T cells?

A
  • T cell receptor (TCR)

* CD4 and CD8 co-receptors

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7
Q

What class of MHC molecule does CD4 “clip onto”?

A

Class II MHC molecule

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8
Q

What class of MHC molecule does CD8 “clip onto”?

A

Class I MHC molecule

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9
Q

For a T cell to be activated what must occur?

A
  • T cell receptors ligated by MHC-peptide

* Co-stimulation signals

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10
Q

What does Toll-like receptor 4 (TLR4) recognise?

A
  • LPS (component of Gram-negative bacteria)

* Proteins from specific viruses

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11
Q

What does Toll-like receptor 2 (TLR”) recognise?

A
  • Molecules that are “signatures” of Gram-positive bacteria
  • Lipopeptides
  • Lipoproteins
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12
Q

What does toll-like receptor 3 (TLR3) recognise?

A

Double-stranded RNA produced during many viral infections

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13
Q

What does Toll-like receptor 9 (TLR9) recognise?

A

Unmethylated DNA dinucleotides CpG (a characteristic of bacterial DNA)

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14
Q

What does Th1 cells (helper T1 cells) protect against?

A
  • Bacterial infection in tissues

* Virus in tissues

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15
Q

What does Th2 cells (helper T2 cells) protect against?

A
  • Parasites via digestive tract

* Pathogenic bacteria via digestive tract

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16
Q

What does Th17 cells (helper T17 cells) protect against?

A
  • Fungi

* Extracellular bacteria

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17
Q

What are the organs of the secondary lymphoid organs?

A
  • Lymph nodes
  • Spleen
  • Mucosal-associated lymphoid tissue (MALT)
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18
Q

What are the steps of the movement of the immune system cells through the lymph node?

A
  • Naïve B cell enter the node expressing chemokine CXCL13. They are attracted to where the follicular dendritic cells are displaying opsonized antigen.
  • Once its cognate antigen is found, CXCL13 is downregulated and CCR7 (chemokine receptor) is upregulated
  • CCR7 detects a chemokine where B and T cells meet (attracted by its “smell”). The B cell receives help from an activated helper T cell
  • The activated helper T cell downregulates expression of chemokine receptors and upregulates CXCR5 chemokine receptors, which attract them to the border of the follicle
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19
Q

What must occur before antibodies can be produced?

A
  • APCs (antigen presenting cells) to present antigen to helper T cells (Th cells)
  • Th cells with receptors that recognise the presented antigen
  • Opsonized antigen displayed by follicular dendritic cells
  • B cells with receptors that recognise the antigen
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20
Q

Where in the lymph node is the killer T cell activated?

A

Paracortex

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21
Q

Where do Peyer’s patches sample antigens from?

A

Intestines (small)

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22
Q

Where does the spleen sample antigens from?

A

Resident dendritic cells in the marginal sinuses of the spleen

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23
Q

What is pneumonia?

A

Consolidation of lung tissue by an inflammatory exudate effusion, usually caused by bacteria

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24
Q

What is pleural effusion?

A

Refers to the collection of fluid in one or both pleural cavities surrounding the lungs

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25
Q

What is the difference between plasma and cerebrospinal fluid?

A
  • Cerebrospinal fluid has less protein and a lower concentration of protein-bound components (bilirubin)
  • Cerebrospinal fluids electrolytes have more chloride and less potassium and calcium than plasma
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26
Q

How is xanthochromia seen?

A

The cerebrospinal fluid has yellow discolouration

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27
Q

When should a lumbar puncture not be performed?

A

When the patient has a raised intracranial pressure from
• Hypertension
• Bradycardia
• Papilloedema

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28
Q

What is chlye?

A
  • Lymph found in the intestinal lymphatics during absorption of food
  • Appears milky due to the presence of fats
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29
Q

What does CTLA-4 (cytotoxic T-lymphocyte-associated protein 4) and PD-1 (programmed death 1) function as?

A
  • Checkpoint proteins which deactivate/“decommission” T cells as the battle winds down
  • CTLA-4 makes it more difficult to reactivate T cells
  • PD-1 make T cells function less well
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30
Q

What are the steps for activating a T cell?

A
  • Cell-cell adhesion
  • TCR clustering
  • Co-stimulation
31
Q

How does Bacteroides fragilis affect toll-like receptors on helper T cells?

A

The TLR recognises polysaccharide A and the T cell is instructed to produce IL-10 which dampens inflammation

32
Q

What does Bifidobacterium breve affect?

A

Dendritic cells produce IL-10

33
Q

Bacteroides fragilis and Bifidobacterium breve are examples of what?

A

Commensal bacteria

34
Q

In response to a serious attack in the intestinal system, what is activated and what does it secrete?

A

• Th1 cells
o Secretes IFN-γ (enhances killing power of lamina propria macrophages)
• Th17 when in an environment of TGFβ and IL-6 or TGFβ and IL-23
o Produce IL-17 (to increase intestinal barriers effectiveness by strengthening the tight junctions between epithelial cells and facilitate transcytosis of IgA)
o Recruits neutrophils from blood stream

35
Q

What does Toll-like receptor 5 (TLR5) indicate?

A
  • Flagellin protein from which flagella are constructed

* Used as a danger signal

36
Q

What causes allergies?

A

Overproduction of IgE antibodies in response to otherwise innocuous environmental antigens (allergens)

37
Q

What can cause autoimmune disorders?

A
  • Genetic defects

* Layer of tolerance-inducing mechanisms fail in eliminating self-reactive cells in genetically normal individuals

38
Q

What must occur to a genetically normal individual for an autoimmune disorder to occur?

A
  • MHC molecules that can present a self-antigen
  • Lymphocytes with receptors that can recognise the self-antigen
  • Environmental factors leading to the breakdown of the tolerance mechanisms designed to eliminate self-reactive lymphocytes
39
Q

What is the molecular mimicry hypothesis?

A

During a microbial invasion, lymphocytes whose receptors recognise microbial antigens will be activated. The molecular mimicry hypothesis holds that sometimes these receptors also recognise a self-antigen, and if they do, an autoimmune response to that self-antigen may result

40
Q

How are the self-reactive lymphocytes activated?

A

Simultaneously from molecular mimicry, the tissue undergoes inflammation by either the microbe itself, another, or an unrelated infection/trauma. This inflammation re-stimulates self-reactive T cells, and this upregulates Class I MHC molecules for a better target of self-reactive lymphocytes

41
Q

What autoimmune disorder is not caused by molecular mimincry?

A

Celiac disease

42
Q

How can a memory killer T cell be produced during a microbial attack?

A
  • The microbe must infect an antigen presenting cell
  • Killer T cells will recognise the virus’s proteins and activate
  • If assistance of helper T cells is available, memory T cells are produced
43
Q

What is a proto-oncogene?

A

A gene which, when mutated, can cause a cell to proliferate inappropriately

44
Q

What does the safeguard system that monitors unrepaired mutations do?

A
  • If mutations are not extensive, the system will stop the cell from proliferating to give the repair system more time to repair
  • If the genetic damage is severe, the system will trigger the cell to commit suicide, eliminating the possibility that it will become a cancer cell
45
Q

What is p53

A
  • A protein of the safeguard system
  • Safeguards against uncontrolled cell growth
  • Known as tumour suppressors
46
Q

What does cancer result from?

A

When multiple systems, both growth-promoting and safeguard, are corrupted within a single cell, cancer results

47
Q

How can PD-1 become impaired by a cancer cell?

A
  • Many types of cancer cells express ligands for PD-1
  • PD-1 is ligated to the cancer cell and supresses the T cells effector function (ability to kill their target cells) and the ability to proliferate
48
Q

Checkpoint blockage cancer treatment only works if a patient is doing what?

A

If the patient’s immune system is producing anti-tumour T cells whose effectiveness is limited wither because there are too few of them or because they do not function well

49
Q

What is an important point of checkpoint blockade cancer treatment?

A

It does not work for all cancers, only for tumour-specific T cell cancers

50
Q

What are some cancer immunotherapies using T cells?

A
  • Adoptive cell transfer

* Engineered T cells (CAR T cell therapy)

51
Q

What are some typical causes of necrosis?

A
  • Tissue trauma
  • Burns
  • Certain toxins
  • Non-physiological stimuli
52
Q

What are some differences between apoptosis and necrosis?

A
  • DAMPs are released in necrosis where in apoptosis DAMPs are hidden
  • Necrosis is uncontrolled cell death where apoptosis is regulated cell death
  • Necrosis encourages an immune response where apoptosis does not active the immune system
  • Necrosis ruptures cells where apoptosis is removed by phagocytosis of macrophages
53
Q

What cells do cytokines effect?

A
  • Endothelium
  • Macrophages
  • Dendritic cell
54
Q

How do cytokines effect the endothelium?

A
  • Cell contraction

* Cytokine secretion

55
Q

How do cytokines effect macrophages?

A

Cell activation

56
Q

How do cytokines effect dendritic cells?

A

Cell differentiation

57
Q

What cells do chemokines effect?

A

Phagocytes

58
Q

How do chemokines effect phagocytes?

A

Cell migration

59
Q

What does Toll-like receptor 1 (TLR1) recognize?

A
  • Lipopeptides

* Lipoproteins

60
Q

What does Toll-like receptor 6 (TLR6) recognize?

A
  • Lipopeptides

* Lipoproteins

61
Q

What does Toll-like receptor 10 (TLR10) recognize?

A

Unknown

62
Q

What does Toll-like receptor 11 (TLR11) recognize?

A

Profilin (Toxoplasma gondii)

63
Q

What must a phagocyte be able to do to complete phagocytosis completely?

A
  • “home onto” the microorganism
  • Adhere to it
  • Respond by the membrane activation that initiates engulfment
64
Q

What is inflammation?

A

The term given to the series of events that surround an immune response and display a number of characteristic features that are collective consequence of the release of cytokines, chemokines, complement fragments and vasoactive amines from macrophages and mast cells upon the initial encounter with a pathogen

65
Q

What are the characteristic features of inflammation?

A
  • Local swelling (oedema)
  • Redness (due to capillary dilation)
  • Pain
  • Heat
66
Q

What is a lysozyme?

A

Also known as muramidase, it is an antimicrobial enzyme that splits the exposed peptidoglycan wall of susceptible bacteria

67
Q

What induces type I interferons (IFNα and IFNβ)?

A

Viral and bacterial infections

68
Q

What immune cell deals with infections within a cell?

A

Natural killer (NK) cells

69
Q

What pathways does natural killer cells kill their target cells?

A
  • Death receptor pathway

* Granule-dependent pathway

70
Q

What do both pathways of killing the target cell of a natural killer cell lead to?

A

Apoptosis

71
Q

What granules does natural killer cells have?

A
  • Serine proteases called granzymes

* Pore-forming protein called perforin

72
Q

Why cannot macrophages phagocytose parasites?

A

Parasites are much bigger than macrophages, making it physically impossible for the macrophage to engulf the parasite

73
Q

What immune cell attacks a parasite?

A

Eosinophil

74
Q

Why does an eosinophil attack against parasites?

A

• Most helminths (parasite) can active the alternative complement pathway allowing C3b to coat them. This coat of C3b allows the adherence of eosinophils at the C3b receptor. If the contact of eosinophils leads to their activation, they will launch an extracellular attack with their granules (cationic protein damaging the parasite membrane)

Clinical Immunology (3 decks)

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