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MBCHB - PRINCIPLES 1 Summary > Immunology > Flashcards

Immunology Flashcards

1
Q

Skin as a physical barrier

A

composed of tightly packed, highly keratinised, multilayered cells

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2
Q

Skin - physiological features

A
  • low pH 5.5
  • low oxygen tension
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3
Q

Skin - sebaceous glands

A

Secrete hydrophobic oils, lysozyme, ammonia, antimicrobial peptide

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4
Q

Mucus - contains

A
  • Contain lysozyme, defensins and antimicrobial peptides - directly kill pathogen
  • Contain lactoferrin - starves bacteria of iron
  • Secretory IgA prevents bacteria and viruses attaching to and invading epithelial cells
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5
Q

Mucus as a physical barrier

A

Mucous membranes line all cavities in contact with external environment

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6
Q

Mucus - Traps

A
  • Traps invading pathogens
  • Cilia traps pathogens and contributes to removal of mucus
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7
Q

Commensal Bacteria as a barrier

A

Symbiotic relationship with host

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8
Q

Innate Immunity - Macrophages

A
  • Phagocytosis
  • Pro/anti-inflammatory
  • Bacterial killing mechanisms
  • Antigen presentation
  • Wound healing and tissue repair
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9
Q

Innate Immunity - Mast Cells

A
  • Pro-inflammatory
  • Parasitic killing mechanisms
    —–Danger signals expressed from damaged cells
    —–Degranulation - Release of preformed pro-inflammatory substances
    —–Gene expression - production of new pro-inflammatory substances
  • Linked to allergy and asthma
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10
Q

Innate Immunity - NK Cells

A
  • Killing of virally infected cells
    —– Activated NKs release perforin proteins, insert into cell killing it
    —– Activated NKs secrete pro-inflammatory mediated
  • Killing of tumour cells
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11
Q

Innate Immunity - Neutrophils

A

Kill by:
- Phagocytosis
— O Dependant - release of ROS granules
— O Independent - release of lysosome granules
- Degranulation - release of granules containing antibacterial proteins into extracellular environment - direct killing of extracellular pathogens
- NETs - immobilise pathogens, prevent spreading, facilitate phagocytosis

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12
Q

What are PAMPs?

A
  • Pathogen associated molecule patterns
  • Expressed by pathogens
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13
Q

What are PRRs?

A
  • Pattern recognition receptors
  • Expressed by inmate immune cells
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14
Q

What is pinocytosis?

A
  • Ingestion of fluids surrounding cells
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15
Q

What is Receptor Mediated Endocytosis?

A
  • Molecules bound to membrane receptors are internalised - generation of adaptive immunity
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16
Q

What is Phagocytosis?

A
  • Intact particles are internalised whole
    • facilitated by opsonisation
      1. Macrophages and neutrophils express PRRs
      2. Receptors bind to PAMPs, signalling formation of phagocytic cup
      3. Cup extends around the target and internalises, forming a phagosome
      4. Fusion with lysosomes forms phagolysosome
    • kills pathogens and degrades contents
      1. Debris are released into extracellular fluid
      2. Pathogen derived peptides are expressed on special cell surface receptors
    • MHC-II molecules
      1. Pro-inflammatory mediators are released
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17
Q

What is Opsonisation?

A
  • Coats pathogens in opsonins facilitating binding so enhances phagocytosis
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18
Q

What are opsonins?

A
  • Small soluble factors
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19
Q

Examples of opsonins

A
  • C3b
  • C reactive protein (CRP)
  • IgM/IgG antibodies
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20
Q

Acute Inflammation - Inflammation promotes?

A
  • Vascular changes
  • Recruitment and activation of neutrophils
  • Bacteria and innate immune cells produce chemical signals that attract neutrophils to site of infection
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21
Q

What is the process of Transendothelial migration?

A
  1. Migration of neutrophils to endothelium near sites of tissue damage/infection
  2. Neutrophils bind to adhesion molecules on endothelial cells
  3. Migration of neutrophils across endothelium
  4. Movement of neutrophils within the cell via chemotaxis
  5. Activation of neutrophil by PAMPs and TNFa
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22
Q

C3 -> C3b + C3a Pathways?

A

Classical pathway
- Activation by antibodies
- IgM and IgG
Mannose binding lectin pathway
- Mannose binding lectin binds to mannose on bacteria
- Activates C3 cleavase
Alternative pathway
- Once C3b is generated and stabilised C3b amplification loop stimulates more C3 cleavage

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23
Q

What does C3b do?

A
  • Cleaves C5 into C5b and C5a
  • Powerful opsonin
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24
Q

What does C5b do?

A
  • Produces pore forming channel which inserts into pathogen membrane/cell wall
  • This is MAC - membrane attack complex
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25
Q

What does C3a and C5a do?

A

AKA anaphylatoxins
- cause acute inflammation
- promote changes in local vasculature, acute inflammation, leukocyte recruitment by:
1. directly activation Mast cells - as release pro-inflammatory mediators
2. acting on local vasculature, increasing permeability, adhesion molecule expression and increase vasodilation

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26
Q

Acquired Immunity - Detection of Pathogens

A
  • B and T cells learn to distinguish between self and non-self
  • Pathogens express unique antigens
  • T and B cells express antigen receptors
    — individual T and B cells express one type of receptor which is specific to a specific antigen
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27
Q

What are Antigens?

A

Any substance that can cause an adaptive immune response by activating T and B cells

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28
Q

What do B cells do?

A
  • Responsible for humoral immune responses
  • Produce antibodies that attack pathogens circulating in blood and lymph
  • Key in defence against extracellular pathogens
  • Develop and mature in bone marrow
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29
Q

What are B cell receptors (BRC)?

A
  • B cells use membrane bound antibodies as receptors to recognise and bind to antigens
  • Antibodies are produced in response to a specific antigen
  • Differing antibodies have differing variable regions
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30
Q

Activation of B cells?

A
  1. Membrane-bound antibodies on the B cells bind to target antigen IgM (or IgD) within the B cell zone of lymph nodes
  2. B cells require 2 signals to become fully active and begin proliferation
    • Antigen
    • Helper signals
  3. Once activated, they clonally proliferate, become either
    • Plasma cell
      • produce low affinity antibodies - IgM
    • Memory B cell
      • germinal centre response
  4. Change class of antibody produced
    • Long lived plasma cells produce IgG
31
Q

What do T cells do?

A
  • Responsible for cellular immune responses
  • Develop in bone marrow and mature in thymus
  • Key role in defence against intracellular pathogens
    • CD4+ T cells
      • key regulators of the entire immune system
    • CD8+ T cells
      • Kill virally infected body cells
32
Q

What are T cell antigen receptors (TCR)?

A
  • T cells can only recognise peptide antigens presented to their TCRs by MHC molecules
  • Each T cell expresses a unique TCR that can bind to only one specific peptide antigen
  • Variable region is formed of a/b TCR chains
33
Q

Activation of T cells?

A
  • Dendritic cells
    • Immature state in normal conditions
    • Express PRRs bind to PAMPs, in presence of pro-inflammatory mediators mature
    • Phagocytoses pathogen antigens, breaking them down into short peptides, loading them into MHC-I and MHC-II molecules onto cell surface
    • Mature dendritic cells after phagocytosis drain into lymph nodes
  • T Cells
    • Require 2 signals to respond to antigens and fully activate
      • Co-stimulatory molecules expressed by dendritic cells
      • Signal 1 is from the peptide antigen/MHC complex
    • Once activated clonally proliferate and differentiate into different effectors
34
Q

What do CD4+ T cells do?

A
  • Naive CD4+ T cell proliferate and activated by antigens and co-stimulation
  • Activated CD4+ T cells diffentiate into CD4+ Effector TH cells
    • TH1 cells
    • TH2 cells
    • TFH cells
    • TH17 cells
    • Regulatory T cells
35
Q

What does Antigen Activated CD4+ T cells (TH0) do?

A
  • secrete T cell growth factor Interleukin 2 (IL-2)
    • induce auto/paracrine mediated proliferation of activated CD4+ and activated CD8+ T cells
36
Q

What does CD4+ Effector TH1 Cells do?

A
  • Enter sites of infection/inflammation
  • Reactivated by infected tissue resident macrophages
    • as express peptide antigens on their surface in complex with MHC-II
  • So TH1 cells secrete pro-inflammatory cytokines, enhancing macrophage mediated killing of internal pathogens
    • as stimulated production of ROS
37
Q

What does CD4+ Effector TFH Cells do?

A
  • Antigen bound to BCR internalised by B cell via receptor-mediated endocytosis
  • Antigen is degraded, peptides are presented in complex with MHC-II molecules on surface
  • TFH cells move into B cell zone of lymph node, are stimulated by B cell
  • Reactivated effector TSH cells stimulate B cells to clonally proliferate and differentiate
    • as TFH cell increase cell surface co-stimulatory molecules and secrete cytokines
38
Q

What does CD8+ T cells do?

A
  • Activated CD8+ cells proliferate and differentiate into Cytotoxic T lymphocytes (CTLs) AKA killer cells
  • CTLs migrate to sites of infection and kill infected host cells
  • Killing of host cells:
    • CTL binds to infected cell
    • CTL programs target for death including DNA fragmentation
      • Secrete contents of cytotoxic granules
    • CTL migrates to new target
    • Target cell dies
39
Q

What does Major Histocompatibility Complex molecules (MHC) do?

A
  • Present peptide antigens to T cells
40
Q

What does MHC-I do?

A
  • expressed on all nucleated cells
  • present peptide antigen son CD8+ T cells
41
Q

What does MHC-II do?

A
  • Expressed only on professional antigen presenting cells (APCs)
    • Dendritic cells
    • Macrophages, B cells
  • Present peptide antigen to CD4+ T cells
42
Q

Immunoglobulins from most to least abundant

A

G
A
M
D
E

43
Q

What does IgG do?

A
  • Dominant immunoglobulin produced during a secondary immune response
  • Agglutination
  • Complement system activation
  • Foetal immune protection
    • IgG are transported directly across the placenta into foetal blood
  • Neutralisation
  • Opsonisation
  • NK cell activation
44
Q

What does IgA do?

A
  • Monomer in serum
    • Neutralisation
  • Dimer when secreted
    • Neonatal defence
      • In breast milk
    • Neutralisation
45
Q

What does IgM do?

A
  • Monomer when bound to membrane, serves as B cell antigen receptor
  • Pentamer when secreted, first immunoglobulin produced in humoral response
    • Present in plasma and secretory fluids
      • Agglutination
      • Complement system activation
46
Q

What does IgD do?

A
  • Monomer when membrane bound, serves as a B cell receptor
    • Mediated B cell activation
  • Secreted not well understood, found in extremely low concentrations in the blood
47
Q

What does IgE do?

A
  • Trigger allergic responses
48
Q

What is agglutination?

A
  • Antibody crosslinks multiple antigens producing clumps of antigens
  • Mediated by specific antigen binding to IgM and IgG antibodies
  • Increases efficacy of pathogen elimination by phagocytic cells
  • Prevents viruses from binding to and infecting host cells
49
Q

What is life-long immunity?

A
  • Once adaptive immune system has recognised and responded to specific antigen it exhibits life long immunity to that antigen
    • Memory CD4+ T cells
    • Memory CD8+ T cells
    • Memory B cells
    • Long-lived plasma cells
50
Q

What is immunisation?

A
  • Process at which individual develops immunity/memory to a disease
    • Deliberate and natural infection
51
Q

What is vaccination?

A
  • Deliberate administration of antigenic material to produce immunity
52
Q

What is active immunity?

A
  • Protection produced by the persons own immune system
  • Can be stimulated by vaccine or naturally acquired infection
  • Usually permanent
53
Q

What is passive immunity?

A
  • Protection transferred from another person or animal
  • Temporary protection that wanes with time
54
Q

What is herd immunity?

A
  • A population can be protected from a certain virus if a threshold of vaccination is reached
  • Primary infection or vaccination has a slower immune response
  • Secondary infection has a faster immune response
55
Q

What are Hypersensitivity reactions?

A
  • An immune response that results in bystander damage to the self
    • Usually exaggeration of normal immune mechanisms
    • Pathological basis for many chronic diseases including, allergy, chronic inflammation diseases and autoimmunity
56
Q

What are the classes of hypersensitivity?

A
  • Type I - intermediate hypersensitivity
  • Type II - Direct cell effects
  • Type III - Immune complex mediated
  • Type IV - Delayed type hypersensitivity
57
Q

What is Type I - Immediate Hypersensitivity?

A
  • Driven by TH2 effector cells
  • Initial exposure
    • Mast cells and basophils have receptors that cause IgE antibodies to bind and display on their cell surface
    • On first encounter with antigen B cells produce antigen specific IgE antibody
    • After allergen has cleared residual IgE antibodies remain on Mast cell and basophil surfaces
  • Reencounter the allergen
    • Allergen binds to IgE coated Mast and basophils causing degranulation
    • Release of vasoactive mediators - histamine
    • Increased expression of pro-inflammatory cytokines and leukotrienes
    • Recruitment and activation of eosinophils
  • Management of IgE mediated allergic disorders
    • Avoidance of allergen
    • Block mast cell activation
    • Preventing effects of mast cell activation
    • Anti-inflammatory agents
    • Adrenaline
    • Immunotherapy
58
Q

What is Type II - Direct cell effects?

A

Mediated by:
- IgM/IgG antibodies directed toward antigens present on cell surfaces or extracellular matrix
- Sensitisation phase
- generation of relevant IgM/IgG antibodies in a classic humoral immune response
- Pathological phase
- Mediated by normal antibody effector functions
- Type IIa reaction
- Destruction of antigen positive cells
- Can be through opsonisation and phagocytosis or complement and Fc receptor mediated inflammation
- Type IIb recaction AKA type VI
- Stimulation of cell surface antigens
- Antibody mediated cellular dysfunction

59
Q

What is Type III - Immune complex mediated?

A
  • Characterised by deposition of immune complexes on various tissues such as wall of blood vessels, glomerular basement membrane of kidney, synovial membrane of joints and choroid plexus of brain
  • Deposition of immune complexes initiate reaction resulting in damage of surrounding tissue and cause inflammation
  • Sensitisation phase
    • Generation of relevant IgG antibodies in a classic humoral immune response
  • Pathological phase
    • formation of soluble immune complexes in circulation
    • activation of normal antibody effector functions
60
Q

What is Type IV - Delayed type immunity

A
  • Driven by CD4+ T cells
    • Activation of T cells by an antigen → proliferation and differentiation of effector TH1 cells leading to macrophage recruitment and activation
  • Classic hallmarks
    • Large number of macrophages at reaction site
    • Takes 24-48 hrs for symptoms to manifest after re-exposure
    • Granulomas often form due to infectious pathogens/foreign bodies that cannot be cleared
  • Sensitisation phage
    • Activation of T cells in a classical adaptive immune response
  • Pathological phase
    • Reactivation of pro-inflammatory effector T cells Th1 in tissues in an antigen specific manner
    • Hyperactiviation of macrophages
    • Secretion of pro-inflammatory cytokines and increased inflammation and tissue damage
61
Q

What are the hallmark features of immunodeficiency?

A

SPUR
- Serious infections
- Persistent infections
- Unusual infections
- Recurrent infections

62
Q

What is X-linked Agammaglobulinemia (XLA)?

A
  • Mutations of BTK gene
  • X-linked recessive inheritance
  • Pathogenesis
    • Block in differentiation and development of B cells and Igs of all types
  • Immunological features
    • Absence or severe reduction in B cells and Igs of all types
63
Q

What is Hyper-IgM Syndrome (HIGM)?

A
  • Caused by a variety of different gene mutations
  • Common cause
    • Mutations in the CD40L gene
  • Pathogenesis
    • Defective interactions between B cells and TFH cells
  • Immunological features
    • Normal numbers of B and T cells
    • Reduced numbers of memory B cells
    • Normal/elevated levels of serum IgM
    • Decreased or normal levels of IgG
64
Q

What is X-SCID?

A
  • X-linked severe combined immunodeficiency
  • Caused by mutations of IL2RG
  • Pathogenesis
    • Failure of T cell and NK cell development and/or function
  • Immunological features
    • Very low or absent T cells and NK cells
    • B cells are usually present but immunoglobin production is severly reduced or absent
65
Q

What is CGD?

A
  • Chronic Granulomatous Disease
  • Caused by mutations in genes coding for NADPH
    • Most common cause p47phox mutations
  • Pathogenesis
    • Defect in generation of oxidative radicals needed by host phagocytic cells
  • Immunological features
    • Free radical deficiency → reduced phagocytic killing by neutrophils and macrophages
66
Q

What are primary immunodeficiency disorders?

A
  • Rare
  • More than 300 distinct immune deficiencies

Tests
- Measuring serum Ig levels
- Measuring the number of peripheral B cells in the blood
- DNA sequencing of genes suspected to be involved

Treatments
- Intravenous Immunoglobin (IVIG)
- Antimicrobial agents

67
Q

What are Secondary Immunodeficiency Disorders?

A
  • Common
  • Subtle
  • Can involve more than one component of immune system

Non-genetic causes of secondary immune deficiency
- Infection
- HIV
- Treatment interventions
- Anti-cancer agents
- Malignancy
- Cancers of the immune system
- Biochemical and nutritional disorders
- Malnutrition

68
Q

What is Autoimmunity?

A
  • Defined as the presence of immune responses against self-antigens

Harmless:
- Low titres of auto-antibodies or auto-reactive T cells

Harmful:
- High titres of auto-antibodies or auto-reactive T cells
- Significant tissue/organ damage, chronic inflammation

69
Q

What is the development of self recognising B and T cells?

A
  • Antigen receptor gene rearrangement in developing T cells and B cells is random
  • Possibility of producing antigen specific receptors that recognise self

Tolerance mechanisms are used to kill or inactivate auto-reactive lymphocytes

  1. Deletion of self-reactive T cells/B cells in primary lymphoid tissues during the early stages of their development
    • AKA central tolerance
  2. Regulatory T cells can help suppress activity/function of self-reactive T cells/B cells in peripheral tissues that escape central tolerance and complete their development
    • AKA peripheral tolerance
70
Q

What are regulatory T cells?

A
  • Suppress lymphocyte activation or function
  • Crucial for suppressing hyper-active or self-reactive T cells
    • Via production of anti-inflammatory cytokines
71
Q

What is the pathogenesis of autoimmune diseases?

A
  1. Genetic susceptibility
  2. Initiation agent
  3. Breakdown of immune tolerance to self-antigens
    • Loss of immune regulation → generation/activation of auto-reactive B and T cells

a. Autoimmune phenomena
b. Autoimmune disease

72
Q

What are the genetic influences in autoimmune disease?

A
  • Monogenic disorders
    • Single gene defects causing autoimmune diseases are rare
  • Most autoimmune diseases result from complex genetic interplay
  • Certain HLA (human leucocyte antigens) have been linked to increased or decreased rick of developing autoimmunity
73
Q

What are the environmental influences in autoimmune disease?

A

Several environmental factors can trigger autoimmunity in genetically predisposed individuals
- Infections
- Cigarette smoking
- Hormone levels
- Tissue damage

Mechanisms
- Molecular mimicry
- Alterations to self-antigens
- Antigen sequestrations
- Bacterial superantigens

MBCHB - PRINCIPLES 1 Summary (5 decks)

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