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Microbiology And Immunology > Hypersensitivity Reactions > Flashcards

Hypersensitivity Reactions Flashcards

1
Q

What is hypersensitivity?

A

An inappropriate immune response to non-infectious antigens that results in tissue damage and disease

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2
Q

State the 4 types?

A
  • Type 1: immediate hypersensitivity/allergy
  • Type 2: cytotoxic hypersensitivity
  • Type 3: serum sickness and Arthus reaction
  • Type 4: delayed-type hypersensitivity, contact dermatitis
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3
Q

State the components required for a type I hypersensitivity reaction and state 3 examples?

A
  • Immune reactant: IgE, Antigen: Soluble antigen (allergen), effector mechanism: Mast cell activation + degranulation via IR + A
  • Example -> Allergic rhinitis, asthma, systemic anaphylaxis
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4
Q

Describe what occurs in the immediate hypersensitivity reaction?

A
  • Antigen enters tissue -> if cross-reactive with mast cells (IgE) -> activation -> release of immune cells -> Activates wheal-flare reaction -> Vasolidation, oedema + swelling of tissue
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5
Q

Describe what type II HS reactions respond to and state the components involved, naming an example of what causes it?

A
  • Respond to altered components of human cells
  • Components -> Immune reaction: IgG (anti-drug ABs), Antigen: Platelet/BC coated with drug, effector mechanism: AB binds cells -> Cleared via macrophages (FcRs) + complement -> kills RBCs -> haemolytic anaemia
  • Example -> drug allergies i.e penicillin
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6
Q

Describe a special type of type II response and state 2 conditions which this occurs in

A
  • IgG antibodies directed at CS receptors -> Antibodies disrupt function via uncontrollable activation OR block receptor
  • Grave’s diseases (TSHR), myasthenia gravis (nACHR)
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7
Q

Describe how haemolytic disease of the newborn is an example of a type lI hypersensitivity reaction?

A
  • HD -> child dies in utero -> via severe haemolytic anaemia
  • Occurs with rhesus (RHD) -ve mother + RHD + ve foetus - First child: Placenta separates from uterus -> exposed to foetal RBC RHD -> maternal sensitisation -> ABs against foetal RBCs produced -> first child unaffected
  • 2nd child -> ABs cross placenta -> into foetal circulation -> Foetal RBCs killed -> haemolytic anaemia
  • If you’re rhesus positive (RhD positive), it means that a protein (D antigen) is found on the surface of your red blood cells
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8
Q

Describe the type of components inolved in type 3 hypersensitivity reactions and state 2 examples?

A
  • Immune reactant: IgG, Antigen: Soluble antigen,
  • effector mechanism: IgG + soluble antigen = immune complex -> activate macrophage, complement, mast cells -> MSC release IF mediators -> IF cells invade site -> increase blood vessel permeability + blood flow -> accumulation of platelets -> occlusion of small blood vessels, haemorrhage + apperance of purpura -> IC cleared via phagocytes
  • Example -> serum sickness + arthus reaction (following diptheria/tetanus vaccine)
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9
Q

What is serum sickness caused by and state examples of these?

A
  • Caused by large IV dose of soluble antigens (drugs) -> immune complex formation -> depositied in tissues (blood vessel walls) -> tissue damage caused via complement activation + IF responses
  • Occurs via -> Antivenon, farmer’s lung (IF of lung -> fibrosis + damage of lungs), 3-HS pneumonitis (dust, bacteria, fungi)
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10
Q

What 2 factors determine the pathology observed in type III HS reactions?

A

Antigen dose + route of delivery

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11
Q

Describe the components involved within Type IV HS reactions and state examples? (PART 1)

A
  • Delayed - Occurs from 24-72 hours - other take <24 hours
  • Type I -> Immune reactant: Th1 (Ag-specific), Ag: Soluble Antigen, effector mechanism: Th1 activation via Ag recognition -> release of IFN-y -> macrophage activation -> release of chemokine, cytokine, cytotoxin -> lesion,
  • Example: Tuberculin reaction (tuberculoid leprosy), Mantoux test
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12
Q

Describe the components involved within Type IV HS reactions and state examples? (PART 2)

A
  • Type II - IR: Th2 (Ag-specific), Ag: soluble Ag, EM: Th2 activation via Ag -> Release of IL-4, IL-5 eotaxin -> eosinophil activation -> release of basic proteins, enzymes, cytokines,
  • Example: Allergic contact dermatitis (nickel), poison ivy
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13
Q

Production of allergen-specific IgE
What is the type I HS reaction defined as?

A

Disease following a response by the immune system to an otherwise innocuous/not-harmful antigen

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14
Q

What is allergen-specific IgE + describe its production?

A
  • First line of defence against worms -> Binds FceR1 on mast cells + preps them to react in presence of antigen
  • Exposure to allergen -> antigen recognition -> DC migration to lymph node Th2 activation -> IL-4/IL-13 release -> activates B cell -> IgE produced -> binds mast cell
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15
Q

What causes allergic sensitisation?

A
  • Exposure to allergen -> nature of allergen, dosage (Increase vs decrease), timing (age), location of priming (in body)
  • Role of pro-allergic DC + cytokines -> convert Th into Th2 cells
  • Genetic predisposition to allergy
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16
Q

State features about common allergens?

A
  • allergens named systematically (after source organism + order discovered)
  • All may have common functionality
  • Received in decreased doses
  • Increased dose exposure = tolerance
17
Q

How does genetics play a role in allergy?

A

Multiple Complex traits + genetics -> contribute to allergy

18
Q

Describe the role of filaggrin and state what condition if there is a lack of filaggrin?

A
  • Maintains skin integrity
  • Defective: Increased risk of Atopic dermatitis -> via increased access for allergen + sensitisation
19
Q

What makes dendritic cells pro-allergic?

A
  • Injury to skin -> induces cytokine production -> Thymic stromal lymphoprotein may switch DC to ‘pro-allergic’ state -> migrate to LN
20
Q

Effector mechanisms of allergic immune response
Describe what happens in the 2nd exposure to the pollen?

A

Initial response -> Pollen-specific IgE binds mast cell -> 2nd exposure -> Acute release of mast-cell contents -> allergic rhinitis

21
Q

Describe what happens to mast cells when activated?

A
  • Resting -> has bound IgE - allergen-specific -> Contains granules (histamine + IF mediators)
  • Activated -> Specific allergen crosslinks IgE -> Release of granule contents -> Different effects on different tissues (GI, airways, blood vessels)
22
Q

Describe different phases in the allergic response with symptoms?

A
  • Early: Mediated via mast cells -> Release of IF mediators -> whezzing, urticaria, sneezing, conjunctivitis
  • Late -> mediated via T cells -> IL-5 (eosinophil activation) + IL-4 (mast cell) + basophils -> further wheezing, sustained blocked nose, eczema
23
Q

State the effector mediators and their effect produced by mast cells in the early and late phase?

A
  • Early: Histamine (Increased vascular permeability + Smooth muscle contraction), leukotrienes (increased VP, SMC, increased mucus secretion), prostaglandins (chemoattractants for T cells, eosinophils + basophils)
  • Late: Cytokines - IL-4/IL-13 (increased Th2 + IgE) + TNF-alpha (increased tissue IF)
24
Q

Describe the features of eosinophils + its 2 effector function?

A
  • Features -> located in the tissues, recruited to allergic reaction sites, express FceRl upon activation
  • Effector functions -> Release highly toxic granule proteins + free radicals upon activation to kill microorganisms/parasites + cause tissue damage
  • Synthesise + release PGs, leukotrienes + cytokines -> amplify the IF response -> via activating epithelial cells + recruiting leukocytes
25
Q

What is the late phase of the IgE-mediated allergic response dependent on?

A
  • Allergen dose, continued synthesis + release of IF mediators -> consists of allergen specific Th2 cells (- chronic allergic IF (type IV HS) -> cells recruit other cells by cytokine release -> increased further release
26
Q

Describe the difference between reaction and sensitisation to an allergen?

A
  • Cognate = Requires some allergen epitope as T cell which presents it
  • Sensitisation: S occurs before R -> Requires presentation of A to T cells by DC + priming of cognate B cells to produce IgE
  • Reaction: occurs -> re-exposure to A + binds preformed IgE on mast cells
27
Q

What is asthma?

A
  • “A State of reversible bronchial hyper-reactivity resulting from a persistent inflammatory process in response to a number of stimuli in a genetically susceptible individual”.
  • Atopic (allergic) or Non-atopic (occupational, exercise induced, noctural asthma, post-bronchiolotic wheeze)
28
Q

State the characteristics of allergic asthma and state common allergens?

A
  • Episodes of wheezy breathing, narrowing of the airways, rapid changes in airway obstruction, severity varies -> slight wheeziness to asthma attack
  • Common Allergens: pollen, HDM plants, some foods
29
Q

Describe the acute and chronic response in allergic asthma?

A
  • Acute -> occurs within seconds -> results in airway obstruction + breathing difficulties -> allergen-induced mast cell degranulation in the submucosa of the airways
  • Chronic -> chronic IF of the airways -> activation of eosinophils, neutrophils, T cells + other leukocytes -> mediators released by these cells cause airway remodelling, permanent narrowing of the airways +~s further tissue damage
30
Q

Describe the changes that occur to the airway in chronic asthma?

A

Contracted Smooth muscle, excess mucus, decreased lumen diameter -> airway obstruction

31
Q

Describe treatments of asthma allergy in the clinic?

A
  • Immunotherapy: Reverses the sensitisation to allergen by means of tolerising exposure -> via Anti-histamine (blocks H1 receptor), mast cell stabilizer (chromoglycate), lipoxygenase inhibitors (montelukast- inhibitors synthesis of specific mediators))
  • Steroids: Act directly on DNA -> increased transcription of anti-IF mediators e.g. IL-10) + decreased transcription of pro-IF mediators (e.g prednisolone)
  • Bronchodilators: Reverse acute effect of allergy on airways (e.g B2 agonist salbutamol)
32
Q

Describe the hygiene hypothesis?

A
  • childhood exposure to germs and certain infections -> develops the immune system -> differentiates harmless from harmful substances
33
Q

Lecture summary

A
  • Allergy is an inappropriate response to otherwise benign antigen
  • 2 important phases:
  • Sensitisation - allergen presented by DC to Th2 CD4 T cells and B cells
  • Reaction - IgE on mast cells cross-linked by cognate antigen leading to inflammation
  • Simple model is that it is a Th2 disease

Microbiology And Immunology (32 decks)

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