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Microbiology and Immunology > Immunopathology > Flashcards

Immunopathology Flashcards

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1
Q

What is Type I hypersensitivity?

A

immediate

IgE, mast cells, and lipid mediators

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2
Q

What is Type II hypersensitivity?

A

antibody mediated

IgM and IgG against cell-bound or extracellular matrix antigens

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3
Q

What is Type III hypersensitivity?

A

immune complex

IgM and IgG immune complex deposition

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4
Q

What is Type IV hypersensitivity?

A

delayed type

CD4 mediated

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5
Q

What is an allergy?

A
  • Type I/immediate hypersensitivity (associated with forms of Type IV)
  • Immune-mediated inflammatory response to common environmental antigenst that are otherwise harmless
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6
Q

What is an atopic individual?

A
  • hihg levels of circulating IgE (normally barely detectible)
    • ths vaires with condition
  • elevated eosinophils in circulation in tissues
  • elevated of Th2 cells secreting IL-4
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7
Q

IgE is specialised to control…

A

Parasites

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8
Q

What are the two phases of immediate (Type I) hypersensitivity?

A
  • sensitization - rapid, usually not noticed
  • response - varies
    • local (common) - rhinitis, bronchoconstriction, conjunctivitis, hives, skin rashes, hay fever
    • systemic (rare) - anaphylaxis
    • immediate and late phase (both may be occuring at once)
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9
Q

What are the 6 main contributors to the immediate/Type I hypersensitivity mechanism?

A
  • allergens (antigens)
  • Th2 cells - switch on B-cells to produce IgE
  • IgE (antibody)
  • FceRI (high affinity FceR) - IgE receptor
  • mast cells - major player, FceRI receptors
  • eosinophils
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10
Q

What are the features of allergens?

A
  • repeated exposure via mucosal route
  • inhaled: highly soluble proteins, carried by small particles
  • ingested: slowly degraded
  • not easily broken down
  • highly soluble in body fluids (causes systemic response)
  • introduced at very low doses (favours Th2 response)
  • allergens are often (not always) enzymes
    • body might mistake them for parasite enzymes
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11
Q

What are the acute and chronic responses to inhaled allergens?

A
  • acute (pollens, Der p 1)
    • rhinitis, conjunctivitis, hayfever
  • chronic (+ danders)
    • asthma
      • shares some delayed type IV features
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12
Q

What is the sensitization mechanism of Th2 activation?

A
  • Low dose Ag via mucosal route
  • APC has taken it up and presented it
  • in presence of IL-4 binds to T cell
  • Differentiates to Th2
  • Th2 produces IL-4, IL-5, and IL-13
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13
Q

What is the sensitization mechanism IgE secretion?

A
  • Th2 interacts with B-cells via CD40 ligand
  • in presence of IL-4 and IL-13
  • induces proliferation
  • induces isotype switching to IgE
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14
Q

How do dendritic cells contribute IL-4 to Th2 differentiation?

A
  • indirectly (do not produce IL-4)
  • some produce IL-33
    • basophils are activated by IL-33 (and allergens) to secrete IL-4
    • production of IgE

this is part of the sensitization phase

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15
Q

How do basophils contribute IL-4 to Th2 differentiation?

A
  • act as APCs
    • express MHC I and II, PRRs
    • interact w/Ag
    • present Ag to CD4 Th2 via MHC II - TCR (signal 1)
      • upregulation of co-stimulatory molecules (CD80/86 - CD28) (signal 2)
      • secrete IL-4 (signal 3)
      • activates Th2 cells

this is part of the sensitization phase

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16
Q

How do dendritic cells and basophils contribute to Th2 differentiation and IgE production in the sensitization phase?

A

dendritic cells

  • proudce IL-33
  • induces basophils to release IL4
  • Th2 differentiation
    • +CD40L, IL-4, IL-5, IL-13 by Th2 cell
    • binds CD40 –> IgE

basophils

  • act as APCs
  • present allergen/Ag on MHC II - binds to TCR on Th2 cell
  • upregulate CD80/86 production - binds to CD28 on Th2
  • upregulate IL-4 secretion
  • Th2 differentiation
    • +CD40L, IL-4, IL-5, IL-13 by Th2 cell
    • binds CD40 –> IgE
17
Q

What are the properties of mast cells?

A
  • mucosal and epithelial tissues, near interacting areas w/infectious agents e.g. blood vessels
  • contain pre-formed granules
  • bind IgE via high-affinity FceR (only receptor that binds Ab not bound to Ag)
    • sensitizes the mast cell
    • surface-bound IgE is very stable (lasts months or years; normal Ab is 24hrs)
  • binding of IgE (Ab) to allergen induces cross-linking of FceRs
  • degranulation (immediate)
    • contain inflammatory mediators
  • synthesis of more inflammatory mediators (lipid mediators, chemokines, cytokines)
18
Q

Activation of mast cells results in:

A
  • secretion of preformed mediators from granules (immediate, 30-45s)
    • histamine, heparin, enzymes (tryptase, chymase), TNF-a
  • synthesis and secretion of lipid mediators on mast cell activation (still immediate, 10-30mins)
    • prostaglandins and leukotrienes from arachidonic acid intermediates
  • synthesis and secretion of cytokines (slow)
    • mast cells make more mRNA for synthesis of cytokines, IL-3, IL-4, IL-13, IL-5, TNF-a
19
Q

What is a wheal and flare response?

A
  • type I hypersensitivity (immediate)
  • immediate phase (seconds to minutes)
  • allergen introduced into skin
  • components released from granules and synthesized by mast cells (e.g. histamines)
  • blood vessels dilate, leak plasma –> swelling, pallor (wheal, squishy)
  • further dilation leads to reddened area from blood (flare)
20
Q

What is the late phase of the wheal and flare response?

A
  • type I/immediate hypersensitivity
  • late phase (8-12 hours)
  • much bigger response by the slowly produced mediators (chemokines, cytokines, leukotrienes)
  • site is full of cells (neutrophils, Th2 cells, basophils, eosinophils)
    • sustained oedema, hard to touch
    • eosinophil presence is characteristic of atopic individuals
21
Q

What are the common allergic responses induced by mast cells?

A
  • vasodilation
  • vasopermeability
  • smooth muscle contraction
  • fluid secretion
22
Q

What is the reaction to the allergic response of mast cells in the GIT?

A
  • +fluid secretion and +peristalsis
  • leads to diarrhea and vomiting
23
Q

What is the reaction to the allergic response of mast cells in the skin?

A
  • +fluid secretion (wheal) and +vasodilation (flare)
  • leads to swelling, itching, urticaria (hives)
24
Q

What is the reaction to the allergic response of mast cells in the airways?

A
  • -broncial diameter, +mucous
  • nasal blockage, coughing, phlegm, asthma
25
Q

What is the reaction to the allergic response of mast cells in the blood vessels?

A
  • +blood flow, +permeability
  • leads to +tissue fluid, +cell infiltrate
  • can lead to anaphylactic shock (systemic)
    • CO cannot keep up with +blood flow to hugely dilated vessels
26
Q

What cell type is characteristic of the late effector phase of type I/immediate hypersensitivity?

A

Eosinophils

  • normally in mucosal linings at low numbers to protect against parasites
  • when activated (late only) they produce toxic granule-derived basic proteins and free radicals responsible for tissue damage and remodelling (meant for parasites, but instead is happening to us)
  • produce chemical mediators that activate local tissues
    • epithelial cell activation, inflammatory cell recruitment and activation
  • normally, tightly controlled; bypassed in allergic responses
27
Q

What happens when eosinophil control is bypassed in late allergic responses?

A
  • part of type I/immediate hypersensitivity late effector phase
  • IL-5 produced by early Th2 cells and by mast cells activates:
    • eosinophils
    • eosinophil production by bone marrow
  • eosinophils are then attracted to and infiltrate tissues (inflamatory chemokines from epithelial cells)
  • activation in tissues:
    • release toxic granules
    • upregulate FceRIs, boosting IgE binding and tf activation and degranulation (increased sensitivity, decreased threshold)
28
Q

What are some symptomatic allergy treatements?

A

these are non-antigen specific treatments

  • adrenaline/epinephrine in anaphylaxis
  • inhaled B-aR agonists in asthma
  • antihistamines for hives, allergic rhinitis
  • corticosteroids
29
Q

What is immunotherapy or desensitization?

A
  • administration of increasing doses of allergen to achieve tolerance
  • induces T-cell tolerance by:
    • -allergen-induced proliferation
    • switch from Th2 response to Th1 response (leads to deviation of secreted cytokines)
    • switch T cells to kill themselves
    • production of Treg cells to control Th2 cells
  • new research is targeting basophils and eosinophils
30
Q

What are the feautres of delayed type/type IV hypersensitivity?

A
  • cell mediated: ++T-cells (particularly Th1, sometimes Th8) and macrophages
  • it is a normal immune response
31
Q

What elicits delayed type/IV hypersensitivity?

A

Persistent antigenic stimulation, e.g.

  • mycobacterium TB
  • mycobacterium perae
  • actinomyces
  • leishmania sp
  • schistosoma sp
  • hep B & C viruses
  • picrylchloride
  • hair dyes
  • nickel salts
  • poison ivy
  • thiomersol
32
Q

What is the mechanism of the sensitization phase in delayed type/IV hypersensitivity?

A

priming of the adaptive response

  • allergen/Ag in skin or mucosa taken up by APCs
  • APCs take it to lymph nodes
  • APCs produce +IL-12:
    • –> T-cell differentiation to Th1
    • –> switches on CD8 T cells
  • CD8 T cells & Th1–> site of allergen/Ag but cannot remove it
  • allergen/Ag persists
  • this process continues on and on
33
Q

What are the 3 main kinds of type IV/delayed type hypersensitivity?

A
  • contact sensitivity (poison ivy, adhesives, tuberculin skin test)
    • usually caused by chemicals
    • previous sensitization, upon re-exposure central and effector memory cells are triggered
  • infection (mycobacterium tuberculosis)
    • inability to clear organism results in persistent activation of Th1 cells
  • non-infectious disease: celiac disease
    • exposure to wheat products induces Th1 dependent immunopathology of intestinal wall
34
Q

What is the mechanism of contact hypersensitivity?

A

sensitization (e.g. poison ivy, pentacdecatechol = Ag)

  • Ag picked up by DCs in skin
  • broken down, displayed on MHC
  • DC drains to local lymph node
  • activates naive T cells
  • T cells migrate back to skin as memory T cells (normal)

response

  • on re-exposure more DCs are activated (as above) AND activation of memory T cells in skin
  • huge increase in T cells at infection site = hard swelling (cells, not fluid)
  • cells produce lots of IFNy (Th1s)
    • massive macrophage activation at inflammatory site
    • v. problematic
35
Q

What is the mechanism of delayed type hypersensitivity responses in TB?

A
  • inhaled in droplets –> alveoli
  • TB (facultative intracellular pathogen) survives in the alveolar macrophages
  • some break down by macrophages, cytokines released (IL-12)
  • DCs take bits of TB to lymph nodes –> Th and CD + IL-12 –> Th1
  • TH1 stimualtes more macrophages via IFNy –> cycle persists
  • prolonged macrophage by IFNy activation produces:
    • IL-8, Il-1, TNFa –> endothelial activation, phagocyte and lymphocyte migration
    • IL-1 –> fever
    • TNFa –> weight loss, granuloma formation
      • contains MNG cells, epithelioid cells, monocytes, CD4s, CD8s
      • normal response, controls infection (90%)
      • can interrupt respiratory/alvelolar function (10%)
        • ​can burst BVs, cause hemoptysis (bloody sputum)
36
Q

What is the mechanism of delayed type/IV hypersensitivity in celiac disease?

A
  • gliadin, breakdown product of gluten (wheat, barley, rye)
    • consists of glutamine & proline
    • +ve glutamine cannot bind gliadin to +ve HLA peptide binding cleft
    • tissue transglutaminase 2 (tTg2) in endomysial cells of intestinal lamina propria deamidate glutamine –> glutamate (-ve)
    • -ve glutamate binds HLA-DQ2 (& DQ-8)
      • >90% CD have HLA-DQ2 MHC
    • APCs under mucosa can bind gliadin
    • APCs –> T cells in MALT –> Th1
    • Th1 –> lamina propria –> ++ IFNy –> activate mø
    • mø release toxic contents, damage villi
      • elongated clefts, ablated villi, +immune cells
  • **we produce Abs to gliadin and tissue transglutaminase
    • used for diagnosis (not involved in disease)

Microbiology and Immunology (9 decks)

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