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PathY5 > Immune response to infections > Flashcards

Immune response to infections Flashcards

1
Q

How do infections get into the body?

A

External Epithelia: Physical contact, wounds and abrasions, insect bites

Mucosal surfaces: Airway, GI tract, reproductive tract

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2
Q

What are the constitutive barriers to infection in the skin?

A
  • Tightly packed keratinised cells
  • Physiological factors (Low pH and Low oxygen tension)
  • Sebaceous glands (Hydrophobic oils, Lysozyme, Ammonia and defensins)
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3
Q

What are the constitutive barriers to infection in mucosal surfaces?

A
  • Secreted mucous (Physical barrier, Secretory IgA, lysozyme/ AntiMicrobial peptides, Lactoferrin)
  • Cilia (trap and move)
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4
Q

What are the constitutive barriers to infection by commensal bacteria?

A

100 trillion normal bacteria

  • Competition
  • Produce fatty acids and bactericidins that inhibit growth
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5
Q

What are the cells of the innate immune system?

A

Polymorphonuclear cells – neutrophils, eosinophils, basophils

Monocytes and macrophages

Natural killer cells

Dendritic cells

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6
Q

What are the soluble components of the innate immune system?

A

Complement
Acute phase proteins
Cytokines and chemokines

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7
Q

What is the cell response in the innate immune system?

A

Essentially identical responses in all individuals

Cells express receptors that allow them to detect and home to sites of infection

Cells express genetically encoded receptors (pattern recognition receptors) that allow them to detect pathogens at site of infection

Cells have phagocytic capacity that allows them to engulf the pathogens

Cells secrete cytokines and chemokines to regulate immune response

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8
Q

What are the polymmorphonuclear cells?

A

Neutrophils, eosinophils, basophils and mast cells

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9
Q

Where are PMNCs produced?

A

Bone marrow

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10
Q

What can PMNCs do?

A

Migrate rapidly to site of injury

Express receptors for cytokines/chemokines - to detect inflammation

Express pattern recognition receptors – to detect pathogens

Express Fc receptors for Ig - to detect immune complexes

Capable of phagocytosis / oxidative & non-oxidative killing – particularly neutrophils

Release enzymes, histamine, lipid mediators of inflammation from granules

Secrete cytokines and chemokines to regulate inflammation

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11
Q

What are the Mononuclear cells?

A

Monocytes and macrophages

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12
Q

What is the difference between monocytes and macrophages?

A

Monocytes are produced in bone marrow, circulate in blood and migrate to tissues where they differentiate to macrophages

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13
Q

What type of macrophage is in the liver?

A

Kupffer cell

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14
Q

What type of macrophage is in the Kidney?

A

Mesangial

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15
Q

What type of macrophage is in the Bone?

A

Osteoclast

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16
Q

What type of macrophage is in the Spleen?

A

Sinusoidal lining

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17
Q

What type of macrophage is in the Lung?

A

Alveolar macrophage

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18
Q

What type of macrophage is in the Neural Tissue?

A

Microglia

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19
Q

What type of macrophage is in the Connective tissues?

A

Histiocyte

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20
Q

What type of macrophage is in the Skin?

A

Langerhans cell

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21
Q

What type of macrophage is in the joints?

A

Macrophage like synoviocytes

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22
Q

Where are macrophages?

A

Tissues

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23
Q

What do macrophages make?

A

Express receptors for cytokines and chemokines - to detect inflammation

Express pattern recognition receptors –to detect pathogens

Express Fc receptors for Ig - to detect immune complexes

Capable of phagocytosis / oxidative and non-oxidative killing

Secrete cytokines and chemokines to regulate inflammation

Capable of presenting processed antigen to T cells

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24
Q

What does cellular damage/ bacterial products trigger?

A

Local production of inflammatory cytokines (activate vascular endothelium enhancing permeability) and chemokines (attract phagocytes)

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25
Q

What are PRR?

A

Pattern recognition receptors such as Toll-like receptors and mannose receptors which recognise generic motifs known as pathogen-associated molecular patterns (PAMPs) such as bacterial sugars, DNA, RNA

Fc receptors for Fc portion of immunoglobulin to allow recognition of immune complexes

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26
Q

What is opsonisation?

A

Opsonins act as a bridge between the pathogen and the phagocyte receptors

Antibodies binding to Fc receptors

Complement components binding to complement receptors

Acute phase proteins eg C reactive protein (CRP)

This allows endocytosis!

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27
Q

How is the phagolysosome?

A

Phagosome and lysosome fuse to form phagolysosome

Protected compartment in which killing of the organism occurs

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28
Q

How does oxidative killing work?

A

NADPH oxidase complex converts oxygen into reactive oxygen species – superoxide and hydrogen peroxide

Myeloperoxidase catalyses production of hydrochlorous acid from hydrogen peroxide and chloride

Hydrochlorous acid is a highly effective oxidant and anti-microbial

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29
Q

How does non oxidative killing work?

A

Release of bacteriocidal enzymes such as lysozyme
and lactoferrin into the phagolysosome

Enzymes present in granules

Each has a unique antimicrobial spectrum

Results in broad coverage against bacteria and fungi

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30
Q

When do neutrophils die?

A

Process of phagocytosis depletes neutrophil glycogen reserves and is followed by neutrophil cell death

> As the cells die, residual enzymes are released, causing liquefaction of closely adjacent tissue.

> Accumulation of dead and dying neutrophils within infected tissue results in the formation of pus

> Extensive localised formation of pus causes abscess formation

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31
Q

What are natural killer cells like?

A

Present within blood and may migrate to inflamed tissue

Express inhibitory receptors for self-HLA molecules that prevent inappropriate activation by normal self

Express a range of activatory receptors including natural cytotoxicity receptors that recognise heparan sulphate proteoglycans

Integrate signals from inhibitory and activatory receptors

Cytotoxic - kill ‘altered self’ as in malignant or virus infected cells

Secrete cytokines to regulate inflammation – promote dendritic cell function

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32
Q

How do you NK cells get triggered into causing lysis?

A

If the inhibitory receptor is not filled by target cell

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33
Q

What are dendritic cells like?

A

Reside in peripheral tissues

Express receptors for cytokines and chemokines - to detect inflammation

Express pathogen recognition receptors – to detect pathogens

Express Fc receptors for Ig - to detect immune complexes

Capable of phagocytosis

Following phagocytosis dendritic cells mature:
Upregulate expression of HLA molecules
Express costimulatory molecules
Migrate via lymphatics to lymph nodes – mediated by CCR7

Present processed antigen to T cells in lymph nodes to prime the adaptive immune response

Express cytokines to regulate the immune response

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34
Q

What are lymphatics?

A

Thoracic duct returns lymph to blood

Naive lymphocytes enter lymph nodes from blood

Antigens from sites of infection reach lymph nodes via lymphatics

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35
Q

What are the parts of the adaptive immune system?

A

Humoral immunity
Cellular immunity
Soluble components

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36
Q

What cells are in humoral immunity?

A

B lymphocytes

Antibody

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37
Q

What are the parts of cellular immunity?

A

T cells - CD4 and CD8

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38
Q

What are the soluble components of adaptive immunity?

A

Cytokines and chemokines

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39
Q

What are the characteristics of the adaptive immune system which are different to the innate immune system?

A
  • Wide repertoire of antigen receptors
  • Exquisite specificity
  • Clonal expansion
  • Immunological memory
40
Q

What is a secondary lymphoid organ?

A

Anatomical sites of interaction between naïve lymphocytes and microorganisms

41
Q

What are the secondary lymphoid organs?

A

Spleen
Lymph nodes
Mucosal associated lymphoid tissue

42
Q

How do T lymphocytes mature?

A

Arise from haematopoetic stem cells

Exported as immature cells to the thymus where undergo selection

Mature T lymphocytes enter the circulation and reside in secondary lymphoid organs

43
Q

What is the difference between CD4 and CD8 T cells?

A 
CD8+ T cells recognise peptide presented by HLA class I molecules
CD4+ T cells recognise peptide presented by HLA class II molecules
44
Q

How does selection and central tolerance work in T cells?

A

> Low affinity for HLA -> not selected to avoid inadequate reactivity

> Intermediate affinity for HLA -> Positive selection (about 10% original cells)

> High affinity for HLA -> negative selection to avoid autoreactivity

45
Q

How does selection occur in T cells for CD4/8?

A

Intermediate affinity for HLA class I -> CD8+ T cells

Intermediate affinity for HLA class II -> CD4+ T cells

46
Q

What are the T cell Subsets?

A 
Th1
Th17
Treg
TFh
Th2
47
Q

What do CD4+ cells do?

A

Recognise
peptides derived from extracellular proteins
presented on HLA Class II molecules (HLA-DR, HLA-DP HLA-DQ)

Immunoregulatory functions via cell:cell interactions and expression of cytokines
Provide help for development of full B cell response
Provide help for development of some CD8+ T cell responses

48
Q

What do CD8+ cells do?

A

Specialised cytotoxic cells

Recognise peptides derived from intracellular proteins in association with HLA class I 
HLA-A, HLA-B, HLA-C

Kill cells directly
Perforin (pore forming) and granzymes
Expression of Fas ligand

Secrete cytokines eg IFNg TNFa

Particularly important in defence against viral infections and tumours

49
Q

What is T cell memory?

A

Response to successive exposures to antigen is qualitatively and quantitatively different from that of first exposure
Pool of ‘memory’ T cells ready to respond to antigen
More easily activated than naïve cells

50
Q

What are Th1 cells?

A

Subset of cells that express CD4 and secrete IFN gamma and IL-2

Help CD8 cells and macrophages

51
Q

What do CD8 T cells express?

A

Express receptors that recognise peptides usually derived from intracellular proteins and expressed on HLA class I molecules

52
Q

What do Tfh cells do?

A

Play an important role in promoting germinal centre reactions and differentiation of B cells into IgG and IgA secreting plasma cells

They are follicular helper cells

53
Q

What are Tregs?

A

Subset of lymphocytes that express Foxp3 and CD25

IL10/TGFb expression, CD25+/ FOXp3+

54
Q

How do B lymphocytes mature?

A

Stem cells -> lymphoid progenitors -> Pro B cells -> Pre B cells -> IgM B cells -> Differentiated B cells (IgE, IgG, IgM)

55
Q

How does central tolerance in B cells work?

A

No recognition of self in bone marrow -> survive

Recognition of self -> Negative selection to avoid autoreactivity

56
Q

How does a Bcell antigen encounter work?

A

Early IgM response -> IgM secreting plasma cell

Germinal centre reaction in LN (CD4+ dependent) -> dendritic cell primes CD4Tcell -> CD4 cell helps B cell differentiation using CD40L:CD40 -> B cell proliferation, somatic hypermutation and isotype switching

High affinity IgG, IgA, IgE secreting plasma and memory cells made

57
Q

How are B lymphocytes activated?

A

B cell receptor (surface expressed Ig) binds to antigen

Some B cells mature to plasma cells secreting IgM

If provided with appropriate signals from CD4+ T cells in secondary lymphoid tissue, stimulated B cells rapidly proliferate

Undergo highly complex genetic rearrangements
Isotype switching to IgG, IgA or IgE

Somatic hypermutation to generate high affinity receptors

Further differentiation
plasma cells which produce IgG, IgA or IgE antibody
long-lived memory cells

58
Q

What are immunoglobulins?

A

Soluble proteins made up of two heavy and two light chains

59
Q

What are the important parts in the heavy chain?

A 
Heavy chain determines the antibody class
IgM, IgG, IgA, IgE, IgD, 
subclasses of IgG and IgA also occur.

Antigen is recognised by the antigen binding regions (Fab) of both heavy and light chains

Effector function is determined by the constant region of the heavy chain (Fc)

60
Q

What is the function of the antibody?

A

Fab: ID pathogens and toxins

Fc: interacts with complement, phagocytes and NK cells

Useful in defence against bacteria.

61
Q

How does B cell memory work?

A

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

  1. Lag time reduced to 2-3 days
  2. Antibody titre increased
  3. Mainly high affinity IgG
  4. Can be independent of CD4+ help
62
Q

What is Pre B cell?

A

Exist within the bone marrow and develop from haematopoietic stem cells

63
Q

What is IgA?

A

Divalent antibody present within mucous which helps provide a constitutive barrier to infection

64
Q

What is IgG secreting plasma cell?

A

Cell dependent on the presence of CD4 T cell help for generation.

65
Q

What is IgM secreting plasma cell?

A

Are generated rapidly following antigen recognition and are not dependent on CD4 T cell help

66
Q

What is a primary lymphoid organ?

A

Include both the bone marrow and thymus; sites of B and T cell development

67
Q

What is the thoracic duct?

A

Carries lymphocytes from lymph nodes back to the blood circulation

68
Q

What is the thymus?

A

Site of deletion of T cells with inappropriately high or low affinity for HLA molecules and of maturation of T cells into CD4+ or CD8+ cells

69
Q

What is the germinal centre?

A

Area within secondary lymphoid tissue where B cells proliferate and undergo affinity maturation and isotope switching

70
Q

What is complement?

A

> 20 tightly regulated, linked proteins

Present in the circulation as inactive molecules

71
Q

Where are complement proteins produced?

A

The liver

72
Q

How does complement work?

A

When triggered, enzymatically activate other proteins in a biological cascade
Results in rapid, highly amplified response

73
Q

What are the 3 pathways of complement activations?

A

Classical (C1/2/4)
MBL (C4/2)
Alternative

They go into C3 and then the Membrane Attack Complex
(Common pathway - C5-9)

74
Q

How does the classical pathway work?

A

Formation of antibody-antigen immune complexes

Results in change in antibody shape – exposes binding site for C1

Binding of C1 to the binding site on antibody results in activation of the cascade

Dependent upon activation of acquired immune response (antibody)

75
Q

How does the Mannose binding lectin pathway work?

A

Activated by the direct binding of MBL to microbial cell surface carbohydrates

Directly stimulates the classical pathway, involving C4 and C2 but not C1

Not dependent on acquired immune response

76
Q

How does the alternative pathway work?

A

Directly triggered by binding of C3 to bacterial cell wall components
eg lipopolysaccharide of gram negative bacteria
teichoic acid of gram positive bacteria

Not dependent on acquired immune response

Involves factors B, I and P

77
Q

What happens after the activation of C3 convertase?

A

Activation of C3 is the major amplification step in the complement cascade

Triggers the formation of the membrane attack complex via C5-C9

78
Q

What does the MAC do?

A

Punches hole sin bacterial membranes

79
Q

What do complement fragments do?

A

Increases 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

Punches holes in bacterial membranes

80
Q

What is C1?

A

Triggers classical pathway via antibody binding

81
Q

What is C3?

A

Triggers C5-9 after being cleaved through classical, alternative or MBL pathways

82
Q

What is C9?

A

Binds to microbial surface carbohydrates to activate the complement cascade in an immune complex independent manner

83
Q

What is MBL?

A

Part of the final common pathway resulting in the generation of the membrane attack complex

84
Q

What is a cytokine?

A

Small protein messengers
Immunomodulatory function
Autocrine or paracrine dependent action
Examples include IL-2, IL-6, IL-10, IL-12, TNF-alpha, TGF-beta,

85
Q

What is a chemokine?

A

Chemotactic cytokines – ie chemoattractants

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

Other examples of chemokines include IL-8, RANTES, MIP-1 alpha and beta.

86
Q

What is oxidative killing?

A

Describes killing mediated by reactive oxygen species generated by action of the NADPH oxidase complex

87
Q

What is pathogen recognition mediated by?

A

Is mediated by Toll like receptors which recognise pathogen associated molecular patterns

88
Q

What is opsonisation mediated by?

A

May be mediated by antibodies, complement components or acute phase proteins and facilitates phagocytosis

89
Q

What is non oxidative killing?

A

May be mediated by bacteriocidal enzymes such as lysozyme

90
Q

What are neutrophils?

A

Polymorphonuclear cells capable of phagocytosing pathogens and killing by oxidative and non-oxidative mechanisms

91
Q

What are NK cells?

A

Lymphocytes that express inhibitory receptors capable of recognising HLA class I molecules and have cytotoxic capacity

92
Q

What are dendritic cells?

A

. Immature cells are adapted for pathogen recognition and uptake whilst mature cells are adapted for antigen presentation to prime T cells

93
Q

What are macrophages?

A

Derived from monocytes and resident in peripheral tissues

94
Q

How does a wide repertoire of antigen receptors occur in the adaptive immune system?

A

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 101^2 receptors

Autoreactive cells are likely to be generated

Mechanisms must exist to delete or tolerise these autoreactive cells

95
Q

What do T cells present on their surface?

A

CD3
CD4 or CD8
TCR

96
Q

What are Th2 cells?

A

Helper T cells

IL-4. 5, 10 and 13

PathY5 (98 decks)

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