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TRANSITION BLOCK 1 > Immunology > Flashcards

Immunology Flashcards

1
Q

What is the difference between INNATE and ADAPTIVE immunity?

A

Innate immunity

  • defence mechanism present from birth
  • non-specific (i.e. same response occurs towards many different pathogens)

Acquired immunity

  • induced by the presence of ‘foreign’ or ‘non-self’ material
  • response unique to the specific substance or pathogen
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2
Q

What immune cells are involved in the NON-SPECIFIC innate immune system

A
  • Macrophages
  • Mast Cells
  • NKCs
  • Neutrophils
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3
Q

What physical barriers does our body already have to prevent infection?

A
  • Skin

- Mucous membranes (Resp, GI and GU tracts)

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4
Q

What are the Primary Lymphoid Tissues of the body and what is their main function?

A

Bone Marrow and Thymus

=> Anatomical sites where white blood cells (leukocytes) are produced

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5
Q

How are pathogens removed from the lymphatic circulation?

A
  • lymph filtered at lymph nodes
  • pathogens are trapped in node before the fluid is returned to venous circulation
  • specialised WBC’s used to destroy the pathogens
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6
Q

What aids lymph fluid transport in the body?

A

Lymph flow = similar to venous flow => requires valves to keep it flowing back to venous angles

  • Breathing
  • Muscle contractions
  • Pulsation in the arteries
  • External compression including:
  • Manual lymphatic drainage
  • Short stretch bandages
  • Gradient compression garments
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7
Q

Where in the body can secondary lymphoid tissues be found and what is their function?

A
  • lymph nodes
  • tonsils
  • spleen
  • Peyer’s patches
  • Mucosa Associated Lymphoid Tissue (MALT)
  • all filter and monitor content of ECF
  • lymphocytes areactivated here during adaptive immune response
  • all tissues contain distinct zones for different types of lymphocytes (T cells vs B cells)
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8
Q

What WBCs are derived from a myeloid lineage?

A

Monocytes => Macrophages and Dendritic Cells

Granulocytes => Neutrophils, Eosinophils and Basophils

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9
Q

What WBCs are derived from a lymphoid progenitor cell?

A
  • T cells
  • B cells
  • Natural Killer (NK) cells
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10
Q

What types of cell can be killed by can Natural Killer Cells?

A
  • tumour cells
  • virally-infected cells
  • antibody-bound cells/pathogens
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11
Q

What is the common purpose of Mast Cells, Eosinophils and Bsaophils?

A
  • release highly inflammatory granules and substances when activated
  • Important in defence against large antibody-coated pathogens that cannot be phagocytosed (e.g. parasites)
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12
Q

Where are Mast cells found, and where are eosinophils and basophils found in comparison?

A
  • Mast cells = in tissues
  • eosinophils and basophils = small numbers in the circulation in healthy, non-allergic individuals
  • May be an increase in number in allergic/asthmatic individuals
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13
Q

What function is common to Monocytes, Macrophages and Neutrophils?

A
  • Phagocytosis
    => ingest and kill extracellular pathogens, dead apoptotic cells and small immune complexes
  • Also source of cytokines which regulate acute inflammatory responses
  • important at sites exposed to external environment (e.g. skin, mucosal surfaces => Resp, GI, GU tracts)
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14
Q

Where are Monocytes found compared to macrophages and neutrophils?

A
  • Monocytes circulate in the blood
  • if they migrate into peripheral tissues they can become tissue-resident Macrophages
  • Neutrophils circulate in the blood but are rapidly recruited into inflamed, damaged and infected tissues
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15
Q

What is the function of dendritic cells and where are they most commonly found?

A
  • phagocytosis
  • APC to help activate T cells
  • present in large numbers in tissues that are in contact with the external environment (e.g. the skin, mucosal surfaces e.g. Resp, GI, GU)
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16
Q

What are the main lymphocyte functions?

A

B cells - antibody production
CD4+ T cells (helper T cells) - secrete cytokines
CD8+ T cells (cytotoxic T cells) - kill tumour cells and virally-infected cells

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17
Q

What is meant by the “soluble” components of the immune system?

A

Soluble (humoral) components:

  • Complement System (30 proteins produced in liver)
  • Cytokines (small proteins and peptides, can act locally or systemically)
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18
Q

Describe the different ways in which cytokines can give off signals

A

Autocrine signals - signalling cell and the target cell can be the same or a similar cells

Paracrine signalling- to local cells => quick response

Endocrinesignalling- to distant cells => slower, long-lasting response.

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19
Q

What properties make the skin a good barrier to infection?

A
  • tightly packed, highly keratinised, multi-layered cells
  • Constantly undergo renewal and replacement
  • low pH 5.5 (acidic)
  • Sebaceous glands secrete hydrophobic oils, Lysozyme, Ammonia, Antimicrobial peptides to protect
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20
Q

What properties make mucosal surfaces (such as the Resp or GI tract) good barriers to infection?

A
  • Secretory IgA prevents bacteria and viruses attaching to epithelium
  • Contains enzymes - Lysozyme, defensins and antimicrobial peptides => directly kill invading pathogens
  • Contains Lactoferrin => this starves invading bacteria of iron.
  • Cilia trap pathogens and help to remove mucous (assisted by sneezing and coughing)
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21
Q

How can extracellular bacteria and fungi be ingested by macrophages?

A

Pinocytosis: Ingestion of fluid surrounding cells

Receptor-mediated endocytosis: Molecule bound to receptors is internalised

Phagocytosis: bacteria are internalised whole.
(facilitated by ‘Opsonisation’)

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22
Q

What is opsonisation? What molecules are able to do this?

A
  • Coating of pathogens by soluble factors (opsonins) to enhance phagocytosis

Examples of opsonins:
- C3b
- C-reactive protein (CRP)
I- gG / IgM

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23
Q

How do phagocytes recognise foreign pathogens?

A

They express Pattern Recognition Receptors (PRRs) on their own cell membrane

These can recognise and bind to Pathogen Associated Molecular Patterns (PAMPs) found on the surface of pathogens

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24
Q

What happens when PRRs on the mast cell membrane bind to PAMPs on a pathogen?

A

Degranulation => Release of pre-formed pro-inflammatory substances

Gene expression => Production of new pro-inflammatory substances

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25
Q

What pro-inflammatory mediators are released during the innate immune response?

A
  • Histamines
  • Nitric Oxide
  • Prostaglandins/Leukotrienes
  • Pro-inflammatory Cytokines e.g. TNF Alpha

these cause acute, local inflammation

26
Q

What are the 3 different complement pathways that will cleave C3 into C3a and C3b?

A
  • Classical Pathway
  • Alternative Pathway
  • Mannose Binding Lectin Pathway
27
Q

Describe what happens in the MBL Complement activation pathway

A

Mannose (found on membrane of pathogen)

  • binds to Mannose Binding Lectin
  • This cleaves C3 into C3a and C3b
28
Q

How are downstream events of the complement system activated?

A
  • C3b is unstable => must be bound to a cell after it is produced
  • Binding of C3b to a pathogen stabilises C3b allowing it to activate downstream complement system
  • if C3b were to bind to a normal human cell, these express inhibitory proteins that prevent C3b from activating complement

=> Complement will only be activated in an infection setting

29
Q

Describe what happens in the downstream complement pathway?

A

Active C3b associates with other proteins
=> produces C5 convertase
=> this cleaves inactive C5 into active C5a and C5b.

  • Active C5b produces a channel in the pathogen membrane/cell wall
    => MAC (membrane attack complex)
    => Salt and water can enter the pathogen via this channel, causing pathogen to swell and burst
30
Q

What are the functions of C3a and C5a?

A
  • add to inflammation by degranulating mast cells and acting on vasculature
31
Q

How do pro-inflammatory signals change the vasculature?

A
  • vasodilation
    => increased blood flow (redness)
  • Tight junctions between endothelial cells are lost
    => vascular permeability (swelling/oedema)
  • Vessels express adhesion molecules on surface of the endothelial cells and
    => adhesion of circulating Neutrophils (recruitment of these into the tissues)
32
Q

Describe the steps of Trans-endothelial migration

A
  • Margination of Neutrophils to the endothelium
  • Binding to adhesion molecules (selectins, ICAM-1) on the endothelial cells.
  • Migration of Neutrophils across the endothelium (diapedesis)
33
Q

Why is CRP a good prognostic indicator of inflammation?

A

CRP

  • Rapidly increases during inflammation (up to 30 thousand fold)
  • Short ½ life, so rapidly disappears once inflammation is resolved
34
Q

What small proteins are released from virally infected cells?

A

interferons

35
Q

What is the function of interferons released from the virally infected cells?

A
  • prevent replication of virus
  • signal to produce anti-viral factors that interfere with viral multiplication
  • signal to neighbouring cells to increase the numbers of MHC class I molecules upon their surfaces
    => T cells surveying the area can identify and eliminate the viral infection
36
Q

A reduced number of which surface molecule causes to NKC to kill the appropriate cells?

A

NK cells respond to levels of MHC Class I
- Reduced levels of MHC class I occurs in virally infected and cancerous cells
=> NKCs are indicated to kill these cells

37
Q

Describe how lymph flows through lymph nodes in order to deposit T and B lymphocytes

A
  1. Lymph flows in via afferent vessels
  2. B cells and T cells enter lymph nodes through high endothelial venules (HEV)
  3. B go into the lymphoid follicle.
  4. T cells stay in the T-cell area of the lymph node and interact with dendritic cells that come in through the afferent lymph
  5. Lymph and lymphocytes leave the node via medullary sinus and efferent lymphatic vessels.
  6. Efferent lymph flows back into blood circulation via the subclavian vein
38
Q

What types of antibody can be membrane bound on B cells in order to look for antigens?

A

IgM or IgD

39
Q

Once activated, what can B cells differentiate into?

A
  • Plasma cells => Produce antibodies

- Memory B cells

40
Q

What signals are required for B cells to clonally proliferate?

A
  • B cell receptor (IgM/D) binds to antigen
  • Th Cells stimulated
  • PRR and PAMP interaction
41
Q

What do B cells form within the lymph node when they clonally proliferate?

A
  • secondary follicle within the B cell zone

=> known as the Germinal Centre

42
Q

Plasma cells which secrete IgM are short lived. TRUE/FALSE?

A

TRUE

43
Q

Why do other antibody classes begin to take over after the initial IgM surge?

A

IgM has low affinity compared to other antibody types

=> not as effective

44
Q

Describe the difference in appearance of IgM when it is membrane bound vs in the plasma

A

Membrane bound = monomer

In plasma and secretory fluids = pentamer

45
Q

What is the main function of IgM and how does this help the immune response?

A

Agglutination

  • anitbodies bind to antigen and then cross bind to each other
  • creates a big clump of bacteria which can all be eliminated in one pass
46
Q

How can IgM and IgG activate complement and which pathway is stimulated?

A

Fc regions on IgM and IgG stimulate Classical Pathway

activates C1 complex

47
Q

What Immunoglobulin is most abundant in the blood and is transferred to the foetus through the placenta?

A

IgG

48
Q

Why can children experience a transient hypogammaglobulinaemia?

A

Maternal IgG wears off and child has not produced enough of their own IgG yet
=> this may cause immunodeficiency

49
Q

Why are IgG antibodies such useful opsonins?

A

They bind to the pathogen membrane

- Phagocytes express a type of Fc receptor that binds specifically to the constant region of the IgG heavy chain

50
Q

IgA is found in which of the body’s secretions?

A
  • saliva
  • tears
  • colostrum and breast milk
  • mucus
  • sweat
  • gastric fluid
51
Q

If IgA is found in secretions where is it also likely to be found platying an important role?

A

Primary defence mechanism at mucosal surfaces

these mucosal surfaces make the secretions that IgA is incorporated into

52
Q

What is different about the way T cells can respond to antigens in comparison to that of B cells?

A
  • T cells can only respond to peptide antigens

- the Antigen receptor on the surface of T cells is specific to ONE antigen only

53
Q

How do T cell receptors “see” antigens?

A
  • antigens must be in complex with MHC molecules for T cell to recognise it
54
Q

MHC Class I present to which type of T cell?

A

CD8 Cytotoxic T cell

55
Q

MHC Class II can present to which cells?

A

CD4 T helper Cells

56
Q

MHC Class 2 can be found on the surface of what types of immune cells?

A

Antigen Presenting Cells (APCs)

  • Dendritic cells
  • Macrophages
  • B cells
57
Q

What are dendritic cells found in the skin usually called?

A

Langerhans Cells

58
Q

Describe how Dendritic cells become APCs

A

phagocytes release broken down pathogen (including antigens)

  • antigens bind to dendritic cells and are phagocytosed again
  • Dendritic cells then incorporate these antigens onto their MHC class I and II surface molecules
59
Q

Where do dendritic cells leave the infected/inflammed tissue and migrate to?

A

Migrate to Lymph nodes to come into contact with relevant T cells

60
Q

T helper cells can differentiate into different effector Th cells. What are the different effector cells and why are there multiple types?

A

Th1
Th2
Tfh
Treg.

Some will stay in Lymph node and some will go out to tissue to help other immune cells
(e.g. Th1 - goes to tissues to stimulate macrophages)

61
Q

What T cell growth factor do CD4 cells secrete and what does this do?

A

IL-2
- autocrine/paracrine signal to other T cells
=> allows both CD4 and CD8 to proliferate and differentiate

62
Q

What is the function of Tfh cells? (T Follicular Helper cells)

A

Move into follicles in lymph nodes and cause B cells to proliferate and make Antibodies

TRANSITION BLOCK 1 (4 decks)

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