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Immunology > 4.1 Immunodeficiency and hypersensitivity > Flashcards

4.1 Immunodeficiency and hypersensitivity Flashcards

1
Q

primary immune deficiency:

A
  • inherited genetic defects in immune response genes
  • typically seen in young animals
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2
Q

secondary immune deficiency​:

A
  • acquired immune deficiency
  • typically seen in adult aniamls
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3
Q

primary innate immune: Canine leukocyte artesian deficiency​ (CLAD)

A
  • occurs as a result of a mutation in CD18 gene
  • CD18 is an integrin (cell-adhesion) molecule necessary for neutrophil extravasation and phagocytosis
  • recurrent bacterial infections in the presence of a marked neutrophil
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4
Q

Without CD18 neutrophils can’t?

A

can’t get out of the blood and get into the infected tissues

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5
Q

primary adaptive immune deficiencies: Equine SCID

A
  • autosomal recessive mutation
  • defect in a DNA repair enzyme required for antigen receptor gene recombination
  • no functional T or B cells
  • highly susceptible​ to infection
  • usually die by 4-6 months from bronchopneumonia / sepsis
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6
Q

If a lymphocyte cant make an antigen receptor what happens?

A

it dies

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7
Q

Foul immunodeficiency syndrome:

A
  • profound​ anemia and immunodeficiency
  • B lymphocyte deficiency and lack of antibody production
  • genetic test now developed to identify carriers
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8
Q

Canine X-linked SCID:

A

Basset hounds and corgis
- X-linked: 50 % of males born to carrier females are affected
-usually die from pneumonia or sepsis

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9
Q

interleukin 2:

A

cytokine responsible for driving the ​proliferation of naive T cells when they recognize antigen

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10
Q

Mutation in IL-2R:

A
  • extra C in code
  • all AA acids that are translated beyond that point are wrong and quicly ​come to a premature STOP codon - short and stumpy
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11
Q

selective IgA deficiency of german shepherds​ associated with:

A
  • IBD
  • anal furunculosis
  • disseminated aspergillosis

**common theme = weak muccossal immunity system

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12
Q

retrovirus-induced immonsuppression:

A

-acquired later in adult life
- FeLV
- FIV

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13
Q

toxin-induced immunosuppression:

A
  • toxic substances
  • drugs
  • lead
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14
Q

can lead to immunosuppression​:

A
  • malnutrition
  • stress
  • chronic disease
  • immunosenescence​ (system fails with age)
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15
Q

___ is an immunosuppressive​ hormone

A

Cortisol​

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16
Q

Immunosuppressive​ drugs:

A
  • corticosteroids
  • ciclosporin
  • chemotherapy drugs

Only given for short periods of time

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17
Q

When to suspect immunodeficiency​?

A
  • animal suffering from repeated infections that relapse following therapy
  • animals infected between 3-12 months of age, especially if known breed-suceptability
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18
Q

immunological tolerance:

A
  • sometimes the immune system deliberately​ ignores or suppresses responses to some antigens
  • strategically​ targeted immune suppression
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19
Q

immune tolerance​: (we don’t want to attack)

A

foreign antigen from HARMLESS environmental component
- food antigen, airborne antigen, contact antigen

self-antigen
- ubiquitous protein, tissue-specific protein

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20
Q

when a foreign antigen pathogen is detected what is expected?

A

immune activation, clearance​ of orgainism

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21
Q

foreign pathogen + immune tolerance =

A

persistent​ infection

22
Q

immune tolleranc​e: mucosal​ disease

A
  • bovine viral diarrhea virus (BVDV)
  • pregnant cow infected –> calf becomes immunotolerent to BVDV and persistently is infected
23
Q

foreign environmental antigen (harmless) + tolerance =

A

healthy

24
Q

foreign environmental antigen (harmless) + immune activation =

A

allergic disease

25
Q

self antigen + tolerance =

A

healthy

26
Q

self antigen + immune activation =

A

autoimmune​ disease

27
Q

central toleranc​e:

A
  • clonal deletion​ of most autoreactive T cells occurs in the Thymus
  • some self-reactive​ T cells are reused and forced to become regulatory T cells (natural Tregs)
28
Q

Thymus decide:

A

what T cells are useful​ nd helpful

29
Q

peripheral tolerance:

A
  • immunological ignorance (T cell never meets antigen
  • clonal anergy​ to harmless antigens in the absence of “danger” signals
  • active suppression by induced Tregs
30
Q

Thymic selection of T cells: borderline

A

can only grow to become regulatory T cells not inflammatory T cells

31
Q

anergic:

A

unresponsive to further antigenic stimulation

32
Q

Active suppression: regulatory T cells

A
  • selected in Thymus (natural Tregs) or developed in secondary lymphoid tissues (induced Tregs)
  • military police of the ​immune system
33
Q

what do regulatory T cells produce?

A

natural immunisuppressive cytokines (ex: IL-10 calm immune system) upon activation

34
Q

hypersensitivity:

A

an inappropriate, hyperactive immune response to an antigen
- tolerance mechanisms fail
- can lead to immune-mediated disease
ex:
harmless environmental antigen = allergy
self antigen = autoimmunity

35
Q

Type 1 hypersensitivity:

A
  • immediate type hypersensativity
  • abnormal production of IgE (Only parasites) to an environmental antigen (allergen)
    -Mast cells become sensitized and when triggered attack as if it were a parasite infection when it isnt
  • ‘anti-parasite’ response upon subsequent exposure to allergen
36
Q

True or false: You CAN’T have an allergic reaction the first time your exposed to something?

A

True, must generate IgE antibodies first and they have to get up to a sufficient concentration and bind to surface mast cells

37
Q

Hypersensativity I: Sensitisation Phase:

A
  • associated with a lack of tolerance for that allergen
  • induction of high levels of T helper 2 cells-driving​ class switching of our B cells towards producing igE
  • igE then coats the surface of the mast cell and becomes sensitized
38
Q

Hypersensativity I: Re- exposure and reaction phase:

A
  • Allergen comes in and binds to surface IgEs
  • Mass cell degranulates and releases loads of cytokines, chemokines, and inflammatory​ mediators like histamine
  • This produces an acute inflammatory reaction

** can see further cellular infiltration from eosinophils which produce inflammatory mediators and make things worse

39
Q

Type II hypersensitivity:

A
  • production of IgM or IgG to cell surface antigens or extracellular matrix proteins
  • “neutralization” blockade of receptors
  • an immunological attack on target cell (opsonization and complement)

Red blood cells (common target)
- neonatal isoerthroysis: mares antibodies attack foul red blood cells
- autoimmune hemolytic anemia

40
Q

Feline infectious anemia:

A

the pathogen doesn’t cause disease the immune system does - when an ​antibody tries to kill the pathogen it loses red blood cells

41
Q

Type III hypersensitivity:

A
  • antibody IgG binding to soluble antigen
  • deposition of immune complexes in blood vessels

Vasculitis: ( inflammatory rxn in blood vessels)
- Drug reaction (antibiotics)
- Wet FIP
- Glomerulonephritis (BV in kidneys)
- immune-mediated polyarthritis

42
Q

Cutaneous drug reaction:

A

Cutaneous vasculitis associated with hypersensitivity (IgG) to some drugs (ex: sulphonamide​ antibiotics

43
Q

Huge problem in hypersensitivity III:

A
  • formation of immune complexes in the vasculature
  • creates degree of clotting
  • leads to fluid leakage into tissues and creates inflammatory reaction at this site
44
Q

Type IV hypersensitivity:

A
  • delayed-type hypersensitivity (DTH)

Either caused by:
- abnormal CD4 T cells:
-abnormal CD 8 T cells:

45
Q

Abnormal CD4 T cells:

A
  • abnormal activation of macrophage in healthy tissues
  • macrophage production of inflammatory mediators and MMP enzymes causes tissue damage
46
Q

Abnormal CD8 T cells:

A
  • killer T cells destroy healthy cells mistakenly thinking that are infected by a virus
  • They think Self antigen is a virus
47
Q

Which hypersensitivities​ are mediated by antibodies?

A

Hypersensativity 1, 2, and 3

48
Q

Hypersensativity Type 4 is mediated by?

A

T cells

49
Q

Hypersensitivity IV: ​sensitization​ phase

A
  • Happens before inflammatory reaction
  • abnormal production of T helper type 1 cell (TH1 Cells)
  • instead of becoming regulatory anti-inflammatory cells they become pro-inflammatory TH1 cells
  • leave lymphoid​ to search for infected macrophage
50
Q

Hypersensitivity IV: re- exposure and reaction

A
  • TH 1 tells macrophage it’s not harmless its a pathogen and needs​ to produce a massive inflammatory reaction
  • local inflammatory response develops at the site and requires T cells to find macrophages and tell them to make cytokine
  • This takes 24-72 hrs for signs of inflammation to appear at this site
51
Q

TB Test:

A
  • delayed-type hypersensitivity​ test
  • measure initial skin thickness
  • inject PPD ( mycobacterium avian and bovine)
  • measure skin thickness again 72 hrs later
52
Q

There are several tolerance mechanisms that try to prevent inappropriate immune reactivity. When they fail we may see:

A
  • pro-inflammatory defense systems come into play in the absence if infection

Immunology (10 decks)

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