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EXAM 1 > Immunology > Flashcards

Immunology Flashcards

1
Q

What are some physical barriers to pathogens

A
  • Skin (Cillia in respiratory tract)
  • Body temperature (Fever)
  • pH
  • Competition (non-pathogenic bacteria in the gut)
  • Host-specificity
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2
Q

What is the complement system

A

A part of the humoral, innate immune system which enhances the ability of antibodies and phagocytic cells to clear microbes. Also promotes inflammation.
* Classical pathway
* Lectin pathway
* Alternative pathway

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3
Q

What do all pathways in the complement system do

A

Produce C3 convertase

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4
Q

Describe the lectin pathway

A
  1. MBL recognises and binds to manose on bacteria cell surface
  2. MASP-2 cleaves C4 -> C4a + C4b
  3. C4b binds to bacteria
  4. C2 binds to c4b
  5. MASP-2 cleaves C2 ->C2a + C2b
  6. C2b remains attached to C4b forming C3 convertase

MBL - Manose-binding lectin

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5
Q

Describe the classical pathway

A

Antibodies come and bind to antigens on microbe surface forming a complex.
1. C1q activates by binding to antigen-antibody complex on microbe
2. C1q cleaves C4 -> C4a +C4b
3. C4b binds to the microbe + C2 comes and binds to C4b
4. C1q cleaves C2 -> C2b remains attached to C4b

  1. Forms C3 convertase
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6
Q

Describe the alternative pathway

A

C3b binds to microbial surfaces
1. Protein B binds to C3b
2. Protein D cleaves B into Bb and Ba
3. Protein Bb remains bound to C3b
4. Forms C3 convertase

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7
Q

What is the function of C3b

A

C3b binds to microbes and opsonizes marking them for phagocytes.

C3b binds to C5: C3 convertase cleaves C5 into C5a and C5b.
* C5a is an inflammatory peptide
* C5b recruits C6, C7, C8 and A LOT of C9 to bind to the microbes cell surface forming pores and ultimately destroying the microbe

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8
Q

How are the complement systems activated

A
  • Classical is activated via the binding of C1 on antibody-antigen complexes.
  • Lectin is activated via MBL binding to manose on microbe cell surfaces.
  • Alternative is activated via C3b binding to C5 on microbes
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9
Q

What are the three outcomes of the complement system

A
  • Opsonization
  • Phagocytosis
  • Lysis
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10
Q

What is the membrane attack complex and what does it do

A
  1. C2b+C4b+C3b = C5 convertase
  2. C5 convertase cleaves into C5a and C5b
  3. C5b recruits C6,7,8,9 to attach to the microbe cell surface and form pores leading to cell lysis
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11
Q

What are the symptoms of inflammation

A
  • Rubor - Redness
  • Dolour - Pain
  • Calor - Heat, fever
  • Tumor - Swelling
  • Loss of function
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12
Q

What is stage 1 of inflammation

A

Neutrophils and monocytes that are attacking the pathogen release Kinin, Prostaglandins, Leukotrienes and Histamine
* Histamines - cause vasodilation
* ∴ More blood
* ∴ More immune cells migrate to the site of inflammation
* Migration, Margination and diapedesis occurs

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13
Q

What is margination and diapedesis

Migration is the same as diapedesis

A

Margination is the binding of leukocytes to the blood stream which is then followed by diapedesis.

Diapedesis is the movement of leukocytes out of the blood circulation and force themselves through small gaps in the endothelium layer to rach the tissue of inflammation.

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14
Q

What is stage 2 of inflammation

A
  • Phagocytes are attracted to microorganisms via chemokines
  • Phagocytes destroy microorganisms
  • Tissue repair - Dead/damaged cells are rebuilt
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15
Q

What is the difference between monocytes and macrophages

A

Monocytes are young macrophages in the blood circulation.

Monocytes differentiate to mature macrophages once migrating out of the circulation.

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16
Q

Describe the process of phagocytosis

A
  1. Microbe is engulfed by macrophages cell membrane
  2. Stored in a phagosome (phacytic vesicle)
  3. Lysosome fuses with phagosome forming a Phagolysosome
  4. Microbe is digested by enzymes
  5. Indigestible material leaves the cell via exocytosis
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17
Q

What are NK cells and how do they work

A

Neutral killer cells are part of the immune system. They consist of an activating receptor and an inhibitory receptor. NK cell activates and kills when the activating receptor is activated.

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18
Q

How are NK cells regulated

A

MHC class 1 is found in all human cell (except for red blood cells). If present, it naturally binds to the inhibitory receptor thereby activating phosphotase to deactivate the ‘killing signal’.

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19
Q

What do NK cells do?

A

They are part of the cell-mediated response.
* When NK cells receive interleukin 12 cytokines from macrophages they release interferon-γ.
* IFN-γ enables macrophages to digest and kill microbes
* NK cells can also binds to virus-infected cells and kill them.

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20
Q

What is the role of MHC class I

A
  • Bind to CD8 positive T-cells (Cytolytic T lymphocytes)
  • Present antigen to them
  • Activate them
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21
Q

What is the role of MHC class II

A
  • Bind to CD4 positive T-cells (T-helper cells)
  • Presents antigen to receptor
  • Activate them
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22
Q

What cell types are good at presenting antigens?

A

Matured dendritic cells

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23
Q

How are antigens captured

A
  1. Antigens are captured by phenotypically immature dendritic cells in the epidermis
  2. Antigen presented on cell surface.
  3. Migrates towards lymph nodes (are T-cell rich)
  4. Maturisation occurs on the way
  5. Matured dendritic cell presents antigen to T-cell after entering lymph node.
24
Q

What is the difference between mature and immature dendritic cells?

A

Immature dendritic cells are specialised for makropinocytosis and phagocytosis but are not good at expression.
Mature dendritic cells are very good at expressing MHC, B7 and adhession-molecules.

25
Q

How are antigens presented via MHC class I complexes

A

Microbe present in infected cell.
1. Broken down to microbial protein and then to an unfolded protein.
2. Further broken down to peptides
3. Peptides travel to ER where they are used during the synthesis of MHC class I.
4. Antigen-MHC 1 complex is formed and travels to the cell surface

  1. MHC class 1 presents antigen to CD8 POSITIVE T-cells
26
Q

How are antigens presented via the MHC complex II pathway

A
  1. Microbe is taken up by the cell via endocytosis -> Endocytic vesicle
  2. ER produces & packages MHC class II into a vesicle
  3. Endocytic vesicle and MHC vesicle fuse resulting in peptide-MHC association
  4. Complex reaches cell surface and presents to CD4 positive T-cells
27
Q

What are the stages of development T-cells undergo

A

Precursor produced at the Bone marrow and then moves to the thymus for further development. At the thymus it undergoes…
* TCR-β and α recombination
* Positive and negative selection

28
Q

What is TCR-recombination

A

A process during T-cell production in which it is exposed to different CD to test affinities. A positive interaction with MHC II will result in CD8 receptors being cleaved leaving the CD4 receptors and vice-versa.

29
Q

What is Positive selection and the process surrounding it

A

Testing MHC binding with the T-cell.
* Strong binding [Negative selection]: Potential to activate T-cell even without antigen presence resulting in autoimmune disease. -> Apoptosis
* No binding: No interaction between the MHC-antigen complex and the T-cell receptor -> Apoptosis
* Weak binding: Positive selection

30
Q

What does the activation of T-cells require

A
  • MHC-TCR
  • CD28-CD80/CD86
  • LFA-1 - ICAM-1
31
Q

Describe the activation & prolifferation of T-cells

A
  1. APC (MHC II&I) binds to naive CDx T-cell
  2. Activation
  3. Release of IL-2
  4. IL-2 binds to IL-2R on other CDx T-cells -> Activates
  5. Prolifferation and differentiation of CDx T-cells
32
Q

What transforms T helper 0 cells to T helper 1

A

Activated dendritic cells and/or infected macrophages release IL-12 which causes Th0 to differentiate to Th1. Th1 releases IFN-γ, TNF, IL-2.
* IFN-γ inhibits Th2 differentiation

33
Q

What causes Th0 to differentiate to Th2

A

Activated mast cells release IL-4. Th2 releases..
* IL-4 (positive feedback loop)
* IL-5
* IL-10

34
Q

What is the difference between Th1 and Th2 cells

Good luck

A

Th1 cells destroy intracellular pathogens and release cytokines IFN-γ and TNF that help with…
* Killing Intracellular pathogens
* NO gas production
* Enabling dendritic cell maturation (More T-cell activation)

Whereas Th2 focuses more on extracellular pathogens and releases IL-4,5,10 that…
* Activation and differentiation of B-cells
* are essential for IgE and Th2 development
* IgA synthesis
* are essential for the differentiation and growth of eosinophils

35
Q

TRUE OR FALSE

Cytotoxic CD8 T-cells require help from CD4 T-helper cells

A

TRUE
CD8 differentiation requires IL-2 which is released by Th1

36
Q

How do Cytotoxic T-cells kill target cells

A
  • Secretory mechanism: Through the release of either perforin or granzyme ofwhich both create pores in the target cells cell membrane
  • Non-secretory mechanism: FasL on the T-cell binds to the Fas receptor on the target -> Signals target apoptosis
37
Q

IgM are the only antibodies that can pass through the placenta and be transfered to an unborn child

A

FALSE
IgG antibodies are the only ones capable of passing through the placenta.

38
Q

Explain what somatic hypermutation is

A

When B-cells are activated, they clone and proliferate. However, as they rapidly proliferate, mutations occur at the DNA that codes for the antigen binding region of the antibodies.
* Alters the antigen affinity
* Gradually, stronger affinity antibodies survive
* This phenomenon is called affinity maturation

Somatic hypermutation leads to Affinity maturation

39
Q

What antibodies do Mature B-cells present

A

IgM and IgD

40
Q

What does a repeat infection induce

A

Memory B-cells are still present and rapidly produce IgG antibodies with high affinity.

41
Q

What antibodies do Memory B-cells produce

A

IgG, IgA, IgE

42
Q

What are the causes of Anaphylactic shock

A
  • Insect bites
  • Horse serum (used in vaccinations)
  • Food allergies
  • Drug allergies
43
Q

TRUE OR FALSE

Anaphylactic shock only involves lung function

A

FALSE
Anaphylactic shock is a whole-body allergic reaction

44
Q

What is happening during an anaphylactic shock

A

Mast cells all over the body release histamines which causes…
* Constriction of the airways = Wheezing
* GIT = Abdominal pain, Diarrhoea, cramps, vomitting
* Vasodilation = Decrease BP, Oedema

  • Fluid can also leak onto alveoli = Pulmonary oedema
45
Q

What is the treatment for anaphylactic shock and what happens

A

Epinephrine injection
* Airways open via bronchodilation
* Raises BP via vasoconstriction

Antihistamines & corticosteroids may be given to further reduce symptoms

46
Q

What drugs taken with first-gen antihimstamines causes additive CNS depression

A

In combination with opoids, sedatives, narcotic analgesics or alcohol will result in further sedation.

47
Q

What are mast cell stabilisers and give examples

A

Drugs that inhibit histamine release by inhibiting chloride channles on mast cells.
* Cromolyn
* Nedocromyl

48
Q

What is the difference between first-gen and second-gen antihistamines

A

First-gen:
* Are lipophilic -> Cross blood-brain barrier -> CNS depression manifesting in the form of sedation.
* Helps with motion-sickness.
* Anticholinergic effects

Second gen:
* Are less lipophilic -> Do not cross blood-brain barrier = No sedation * No anti-motion sickness
* No anticholinergic effects

49
Q

What are common side effects associated with first-gen antihistamines

A

CNS depression manifesting as sedation and anticholinergic/antimuscarinic effects including…
* Dry mouth
* Blurred vission
* Constipation
* Urinary retention

50
Q

What are mast cells and how do they function

A

Cells that express FcεRI receptor which is sensetive to IgE antibodies. The binding of IgE and an allergen causes the release granules that contain histamines (degranulation). The histamines cause inflammation and a hypersensetive reaction (allergy)

51
Q

What are the different outcomes of mast cell activation

A

Outcomes depend on the location of activation.
* Gut -> Diarrhoea & vomitting
* Airway -> Wheezing, coughing
* Blood vessels -> Vasodilation (increase blood flow) and increased permeability resulting in oedema

52
Q

What antibody causes an allergic response

A

IgE

53
Q

How is IgE produced/released

A

When allergens, instead of antigens, bind to mature B-cells.

54
Q

What are the different types of receptors histamines function at

A
  • H1 at Smooth muscle, Endothelium and sensory nerve endings
  • H2 at blood vessel smooth muscle
  • H4 at eosinophils
55
Q

What are the different causes of histamines

A
  • Enhanced gastric acid secretion
  • Tachycardia
  • Skin reation (inflammation)
  • Decreased BP via vasodilation
  • Broncho-spasms -> Bronchoconstriction
  • Cardiac arrest (if left untreated)
56
Q

What causes type IV hypersensetivity

A

Activated T-cells with antigen

EXAM 1 (10 decks)

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