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Immunology Path Year 5 > Immune response to infection > Flashcards

Immune response to infection Flashcards

1
Q

What are the constitutive barriers for pathogens to enter our bodies?

A
  1. Skin
    i) Tightly packed keratinised cells
    - > Physically limits colonisation by microorganisms

ii) Physiological Factors
- > Low pH
- > Low Oxygen Tension

iii) Sebaceous Glands
- > Hydrophobic Oils repel water and microorganisms
- > Lysozymes destroy structural integrity of bacterial cell walls
- > Ammonia and Defensins have anti-bacterial properties

  1. Mucosal Surfaces
    i) Secrete mucous
    -> Physical barrier to trap invading pathogens
    Contains:
    - Secretory IgA; prevents bacteria and viruses attaching to and penetrating epithelial cells
    - Lysozyme and antimicrobial peptides; directly kill invading pathogens
    - Lactoferrin; acts to starve invading bacteria of iron

ii) Cilia
- > directly trap pathogens and contribute to removal of mucous, assisted by physical manoeuvres such as sneezing and coughing

  1. Commensal Bacteria
    - > Found throughout skin and mucous membranes
    - > 100 trillion bacteria normally reside at surfaces
  • Compete with pathogenic microorganisms for scarce resources
  • Produce fatty acids and bactericidins that inhibit the growth of many pathogens
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2
Q

What are the different types of cells of the innate immune system?

A
  1. Polymorphonuclear Cells
  2. Mononuclear Cells
  3. Dendritic Cells
  4. Natural Killer Cells
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3
Q

What are polymorphonuclear cells? And what kind of receptors do they have?

A

background

  • > neutrophils + eosinophils + basophils/mast cells
  • > Produced in bone marrow
  • > Migrate rapidly to site of injury

what they have

  • > Express receptors for cytokines/chemokines – to detect inflammation
  • > Express Fc receptors for Ig – to detect immune complexes
  • > Express pattern recognition receptors – to detect pathogens
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4
Q

What are mononuclear cells? What receptors do they have?

A

background

  • > monocytes and macrophages
  • > produced in the bone marrow, circulate in blood, and migrate to tissues and differentiate to macrophages
  • > different names based on the tissue they are in

what they have

  • > Express receptors for cytokines/chemokines – to detect inflammation
  • > Express Fc receptors for Ig – to detect immune complexes
  • > Express pattern recognition receptors – to detect pathogens
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5
Q

What are dendritic cells? What receptors do they have?

A

background

  • > Innate/Adaptive Transitional Cells
  • > Reside in peripheral tissues

what they have

  • > Express receptors for cytokines/chemokines – to detect inflammation
  • > Express Fc receptors for Ig – to detect immune complexes
  • > Express pattern recognition receptors – to detect pathogens
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6
Q

What are natural killer cells? What kind of receptors do they have?

A

background

  • > type of lymphocyte
  • > Present within blood and may migrate to inflamed tissue

what they have

  • > inhibitory receptors for self-HLA molecules that prevent inappropriate activation by normal self
  • > A range of activating receptors including natural cytotoxicity receptors that recognise heparin sulfate proteoglycans
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7
Q

what are three phagocytes?

A
  • > Macrophages
  • > Neutrophils – RESPIRATORY BURST
  • > Dendritic Cells
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8
Q

how are phagocytes recruited?

A
  • > Following infection, there is cellular damage and bacterial products trigger the local production of inflammatory cytokines and chemokines
    i) Cytokines activate vascular endothelium enhancing permeability
    ii) Chemokines attract phagocytes; typically the latter 2 as macrophages reside in tissue
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9
Q

How do phagocytes recognise Microorganisms?

A
  • > Phagocytes can either directly recognise pathogens using PAMPs or recognise the Opsonins that have coated them
    i) PAMPs - Toll like receptors and mannose receptors - bind to PAMPs such as bacterial sugars, DNA and RNA
    ii) Opsonins i.e. Antibodies & Fc Receptors, Complement and Complement Receptors, APP i.e. CRP
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10
Q

How do phagocytes kill Microorganisms?

A

The phagocyte endocytoses the pathogen to form a phagosome. The phagosome then fuses with a lysosome to form a phagolysosome.

i) Oxidative Killing
1. NADPH oxidase complex converts oxygen into ROS (superoxide and hydrogen peroxide)
2. Myeloperoxidase catalyses production of HCL from Hydrogen Peroxide and Chloride
3. HCL is a highly effective oxidant and anti-microbial

ii) Non-Oxidative Killing
Release of bactericidal enzymes such as lysozyme and lactoferrin into the phagolysosome

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11
Q

What is unique about the three phagocytes?

A

Macrophages - survive after phagocytosis and behave as APC
Dendritic Cells - Primary function is to act as APC and transition between innate and adaptive
Neutrophils - Die post phagocytosis. As they die they release enzymes causing liquefaction - pus.

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12
Q

What are the characteristics of cells of the adaptive immune system? (4)

A

Immunological Memory
-> Following infection, residual pool of specific cells with enhanced capacity to response if re-infection occurs

Wide repertoire of antigen Receptors

  • > Receptor repertoire is not entirely genetically encoded
  • > Genes for segments of receptors are rearranged and nucleic acids deleted/added at the sites of rearrangement almost randomly
  • > Potential to create in order of 10^11 to 10^12 receptors
  • > Autoreactive cells are likely to be generated; Mechanisms must exist to delete or tolerise these autoreactive cells

Clonal Expansion

  • > Cells with appropriate specificity will proliferate during infection
  • > T Cells will proliferate into their various effector cells (cytokine secreting, cytotoxic)
  • > B Cells will proliferate into T Cell Independent (IgM) plasma cells, until germinal centre reactions occur to which they form IgG/A/E plasma and memory cells

Exquisite Specificity
-> Able to discriminate between very small differences in molecular structure

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13
Q

What are the characteristics of cells of the innate immune system? (5)

A
  1. Essentially identical responses in all individuals
  2. Cells express receptors that allow them to detect and home to sites of infection
  3. Cells express genetically encoded receptors that allow them to detect pathogens at site of infection
  4. Cells have phagocytic capacity that allows them to engulf pathogens
  5. Cells secrete cytokines and chemokines to regulate immune response
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14
Q

What are Primary lymphoid organs?

A

Organs involved in lymphocyte development

  • > Bone marrow: both B and T lymphocytes are derived from haematopoietic stem cells; site of B cell maturation
  • > Thymus: site of T cell maturation; most active in the foetal and neonatal period; involutes after puberty
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15
Q

What are Secondary lymphoid organs?

A

Anatomical sites of interaction between naïve lymphocytes and APC – where the immune reaction occurs

  • > Lymph nodes
  • > Mucosal associated lymphoid tissue
  • > Spleen
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16
Q

How do T Lymphocytes develop?

A

-> At the Bone Marrow; Stem Cells -> lymphoid progenitors -> pre T cells -> enter circulation towards the thymus
·> At the Thymus; The pre T Cells mature, proliferate and undergo +ve and-ve selection before being exported to the periphery

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17
Q

How does T lymphocyte selection occur?

A

T Cells express both CD3 and their T Cell Receptor
At the Thymus, they encounter a APC with a peptide presented on its HLA (Dendritic Cell)

IF T Cell Receptor has a low affinity for the HLA
-> Deleted due to inadequacy

IF T Cell Receptor has a high affinity for the HLA
-> Deleted due to risk of autoreactivity

IF T Cell Receptor has a moderate affinity for the HLA (around 10% of the T Cells)

i) HLA Class I - Drives CD8+ T Cells
ii) HLA Class II - Drives CD4+ T Cells

IL-2 is KEY TO T-Cell Proliferation and Survival

18
Q

What are CD8+ T cells?

A

Cytotoxic T Cells
These are specialised cytotoxic cells
-> Recognise peptides derived from intracellular proteins in association with HLA class I: HLA-A, HLA-B, HLA-C, found on all cells.

19
Q

What are CD4+ T cells?

A

Helper T Cells
These are specialised immunomodulatory cells
-> Recognise peptides derived from extracellular proteins in association with HLA class II molecules (HLA-DR, HLA-DP, HLA-DQ), expressed typically on APC but can be expressed on others under stress.
-> Helps both B Cells and CD8+ T Cells.

There are a wide variety of Helper T Cells which arise from Cytokine Derived Differentiation

i) Th1 - Secrete IL2, IL10, IFN gamma and TNF alpha. Helps CD8 T Cells and Macrophages
ii) Treg - Secretes IL10, Foxp3, CD25
iii) TFh - Plays an important role in germinal cell reactions differentiating B Cells into IgG and and IgA secreting plasma cells.

iv) Th2 - Secretes IL 4, 5, 10, 13 – ALLERGIC DISEASES
v) Th17 - Secretes IL 17, 21, 22. Helps neutrophil recruitment and autoantibody differentiation
vi) TPh - Peripheral helper T Cells.

20
Q

How does T lymphocyte memory work?

A
  • > Response to successive exposure to antigen is qualitatively and quantitatively different from that of first exposure
  • > In primary T cell response there is a delay, then a peak, then cells die off, but there is residual pool of memory cells left with enhanced reactivity so they can respond more quickly and efficiently to successive infection (more easily activated than naïve cells)
21
Q

How do B lymphocytes develop?

A
  • > At the Bone Marrow; Stem Cells -> lymphoid progenitors -> pre B cells
  • > At the Bone Marrow; The pre B Cells mature, proliferate and undergo +ve and-ve selection before being exported to the periphery
22
Q

How does B lymphocyte selection occur?

A

IF no recognition of self in bone marrow
-> Survive

IF recognition of self in the bone marrow
-> Deletion to avoid autoreactivity

23
Q

How do B lymphocytes mature?

A

i) Run of the mill - IgM
- > After selecting for central tolerance, the B Cell differentiates into IgM secreting Plasma Cells

ii) Further maturation - IgG/A/E
- > At the Germinal Centre of the Lymph Nodes, the B Cells can further Specialise
- > DEPENDENT ON TFh CD4+ T Cell (primed by DC) via CD40L:CD40
- > B Cells proliferate, undergo somatic hypermutation (i.e. increase the affinity of their receptors) -> Become IgG/A/E

24
Q

What are immunoglobulins?

A
  • > Soluble proteins made up of two heavy and two light chains
  • > Heavy chain determines the antibody class (IgM/G/A/E/D) – subclasses of IgG and A also occur
  • > Antigen is recognised by the antigen binding regions (Fab) of both heavy and light chains
25
Q

What do immunoglobulins do?

A
  • > Identification of pathogens and toxins (Fab mediated)
  • > Interact with other components of immune response to remove pathogens (Fc mediated) – complement, phagocytes, NK cells
  • > Particularly important in defence against bacteria of all kinds
26
Q

How does B lymphocyte memory work?

A

-> Response to successive exposure to antigen is qualitatively and quantitatively different from that of first exposure

  • > Primary immune response includes early IgM response and delayed IgG response, but in secondary exposure there is already a population of IgG expressing plasma cells therefore
    i) the lag time between antigen exposure and the production of antibody is decreased to 2-3 days
    ii) the titre of antibodies produced is greatly increased
    iii) the response is dominated by IgG antibodies of high affinity

The response may be independent of help from CD4+ T lymphocytes

27
Q

What is complement?

A
  • > Over 20 tightly regulated, linked proteins produced by liver and present in circulation as inactive molecules
  • > When triggered, enzymatically activate other proteins in a biological cascade – results in rapid, highly amplified response
28
Q

What is the purpose of complement?

A

i) The Membrane Attack Complex forms holes in membranes

ii) The fragments of the complement activation cascade have a wide variety of roles i.e.
- > Inc. vascular permeability and cell trafficking to site of inflammation
- > Opsonisation of immune complexes keeps them soluble
- > Opsonisation of pathogens to promote phagocytosis
- > Activates phagocytes
- > Promotes mast cell/basophil degranulation

29
Q

What are the 3 pathways for complement activation?

A
  1. Classical Pathway
  2. Mannose Binding Lectin Pathway
  3. Alternative Pathway

All the three pathways below act together to activate C3 Convertase

  • > Activation of C3 is the major amplification step in the complement cascade
  • > Triggers the formation of the membrane attack complex via C5-9
30
Q

What is the classical pathway?

A
  1. Classical Pathway - Dependent on adaptive immune response
    - > Activated by the formation of antibody-antigen immune complexes
    - > The complex formed, results in a change in the antibody shape – exposing the binding site for C1
    - > Binding of C1 to the binding site on the antibody activates the cascade
31
Q

What is the mannose binding lectin pathway?

A
  1. Mannose Binding Lectin Pathway - Not dependent on adaptive immune response
    - > Activated by the direct binding of MBL to microbial cell surface carbohydrates
    - > Directly stimulates the classical pathway, involving C4 and C2 but not C1
32
Q

What is the alternative pathway?

A
  1. Alternative Pathway - Not dependent on adaptive immune response
    - > Directly triggered by binding of C3 to bacterial cell wall components e.g. lipopolysaccharide of gram –ve bacteria, teichoic acid of gram +ve bacteria
    - > Involves factors B, D and Properidin
    - > Factor H - Control Protein
33
Q

What are cytokines?

A
  • > Small protein messengers
  • > Immunomodulatory function
  • > Autocrine or paracrine dependent action
  • > e.g. IL-2, IL-6, IL-10, IL-12, TNF-a, TGF-b
34
Q

What are chemokines?

A
  • > Chemotactic cytokines i.e. chemoattracts
  • > Direct recruitment/homing of leukocytes in an inflammatory response
  • > CCL19 and CCL21 are ligands for CCR7 and important in directing dendritic cell trafficking to lymph nodes
  • > Others; IL-8, RANTED, MIP-1 a and b
35
Q

What do polymorphonuclear cells do?

A

what they do

  • > Capable of phagocytosis/oxidative and non-oxidative killing (NOTE; NEUTROPHILS DIE POST KILLING)
  • > Secrete cytokines and chemokines to regulate inflammation
  • > Release enzymes, histamine, lipid mediators of inflammation from granules i.e. myeloperoxidase, defensins and neutrophil elastase - DEGRANULATION
36
Q

What do mononuclear cells do?

A

what they do

  • > Capable of phagocytosis/oxidative and non-oxidative killing
  • > Secrete cytokines and chemokines to regulate inflammation
  • > Capable of presenting processed antigens to T Cells
37
Q

What do dendritic cells do?

A

what they do

  • > Capable of phagocytosis HOWEVER the DC then matures
    i) Upregulate expression of HLA Class 1 ?HLC Class 2. molecules and present antigens on its surface
    ii) Express costimulatory molecules
    iii) Migrate via lymphatics (mediated by CCR7) to lymph nodes

they have one main job;
PRIME THE T-CELLS.

38
Q

What do NK cells do?

A

what they do

  • > If you lose inhibitory signals via HLA down-regulation, then NK cells know something is wrong, they then become activated and they can kill altered self cells i.e. malignant or virus-infected cells
  • > Secrete cytokines to regulate inflammation: promote dendritic cell function
39
Q

How do CD8+ T cells kill cells?

A
  • > Kill cells directly through many mechanisms; particularly important in defence against viral infections and tumours
    i) Perforin (pore forming) and granzymes
    ii) Expression of Fas ligand
    iii) Secrete cytokines e.g. IFN-y, TNF-a

They require assistance from ‘Th1’ Cells to fully achieve their potential.

40
Q

A) Which CD4 T cell helps CD8 T Cells and Macrophages?
B) Which CD4 T cell plays an important role in germinal cell reactions differentiating B Cells into IgG and and IgA secreting plasma cells?

A

A) Th1 - Secrete IL2, IL10, IFN gamma and TNF alpha. Helps CD8 T Cells and Macrophages

B) TFh (T follicular helper) - Plays an important role in germinal cell reactions differentiating B Cells into IgG and and IgA secreting plasma cells.

Immunology Path Year 5 (2 decks)

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