Immunity Flashcards

(45 cards)

1
Q

innate

A

non-specific, no memory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

innate immunity - major components

A

epithelial barriers
phagocytic cells
innate lymphoid cells
plasma proteins - complement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

innate immunity - cellular components

A

phagocytes -
monocytes/macrophages - fever and t cell and macrophage activation, lymphocyte activation, increased antibody prodcution, induce acute phase protein production
neutrophils
eosinophils
basophils
mast cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

innate immune system - secreted components

A

complement - increased vascular permeability, formation of ILs and TNF
cytokines - promote leukocyte cheomtaxis
lysozome
acute phase proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

adaptive immunity

A

specific
remembers pathogens
cell mediated and humoral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

adaptive immunity - cellular components

A

B cells/plasma cells - make antibodies and memory cells
T cells -
CD4 - helper cells - make cytokines, activate other immune cells, inhibit immune function
CD8 - cytotoxic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

adaptive immunity - secreted components

A

antibodies
cytokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

immune recognition of pathogens

A

PAMPs/DAMPs –> activate pattern recognition receptors

PRRs classifications -
secreted - bind microbial surface - activate complement, enable phagocytosis
transmembrane - in cell membrane - macrophages, NK cells, dendritic cells
cytosolic - in cytoplasm of cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

toll-like receptors

A

mediate inflammation in gut
bind bacterial lippolysaccharides
activate signal cascade that regulates inflammatory responses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

dendritic cells

A

antigen presenting
phagocytic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

T helper cells (CD4)

A

Th1 -
activated by IL-12 and IL-18
produce IL-2, IFN-gamma and TNF-beta
direct cell mediated response

Th2 -
activated by IL-4
produce IL-3-6,10, and 13
direct humoral response

also Th17 and T-regs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

FIP - immunopathogenesis

A

antibody production counter productive - enhance uptake and replication in macrophages

–> type 3 hypersenstivity

vaccination makes it worse

effusive - failure to mount T cell immunity in face of vigorous B cell response
dry form - partially effective cell mediated response keeping virus to smaller number of macrophages

dry form always after brief spell of effusive disease

terminal stage - immunity collapses and disease reverts to effusive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

failure of passive immunity

A

dam –> neonate in colostrum (IgG)

failure predisposes neonates to systemic infection - eg joint ill

measured -
indirect - serum total protein, zinc sulphate turbidity
direct - ELISA (foals)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

antibodies

A

B cells –> plasma cells –> produce immunoglobulins

5 classes -
IgG - most abundant - bloodstream and colostrum - small so can go into interstitial spaces
IgM - large - mostly in bloodstream, more antigen binding ability than IgG
IgA - mucosal surfaces and milk
IgE - produced by plasma cells, high affinity for tissue mast cells, involved in allergy
IgD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

primary lymphoid organs

A

antigen independent formation of lymphocytes

thymus
bursa of fabricus
bone marrow
peyers patches in ruminants
foetal liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

secondary lymphoid organs

A

antigen dependent formation of lymphcytes

spleen
tonsil
peyers patches in species other than ruminants
lymph nodes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

tertiary lymphoid organs

A

MALT/GALT/BALT
sampling of pathogens at epithelial surfaces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

primary and secondary immunodeficiency

A

primary - genetic deficiency in a component of the immune system

secondary - exogenous causes of defective immunity - infectious, radiation, chemotherapy, nutritional

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

severe combined immunodeficiency disease (SCID)

A

Different genetic defects - x-linked, autosomal recessive, sporadic

affects both cell mediated and humoral adaptive immunity

arabian horses - autosomal recessive –> lymphopenia and agammaglobulinemia –> death due to secondary infection
marked thymic response

20
Q

chediak higashi syndrom

A

defective ability to release intracellular granules and reduced ADP storage

affects all granulocytes, melanocytes and platelets

21
Q

leukocyte adhesion deficiency

A

dogs (irish setters) and cattle (holsteins)

CD18 deficiency

high numbers of circulating neutrophils but can’t penetrate endothelium

22
Q

fell pony syndrome

A

foal immunodeficiency
autosomal recessive

severe anemia and B cell lymphopenia

23
Q

grey collie syndrome

A

cyclic neutropenia
autosomal recessive
neutrophil count drops

24
Q

Parvovirus (canine parvo and feline panleukopenia)

A

destruction of gut/bloodstream barrier –> consumption of immune factors –> direct infection of immune cells –> lymphocytes destroyed

diarrhoaw
secondary bacterial infections
panleukopenia

25
hypersensitivity
altered injurious immune reactivity to a specific antigen in a sensitised host general features - response elicited by antigens - endogenous, exogenous, or non-microbial imbalance of effector and control mechanisms associated with susceptibility genes poorly controlled normal effector mechanisms cause tissue injury mechanisms sensitisation and effector phases
26
type 1 hypersensitivity - Allergic
previously sensitised individual antigen binds to IgE antibody on mast cell surface excessive Th2 response promotes inflammation systemic or local reaction 2 phase - intermediate - vasodilation, vascular leakage, smooth muscle spasm, gland secretion late - infiltration with leukocytes and destruction of mucosal epithelium local immediate hypersensitivity reactions systemic anaphylaxis - vascular shock, oedema, respiratory distress mediators - histamine enzymes proteoglycans arachidonic acids cytokines diagnosis - signs mast cells tryptase post mortem - acute cardiogenic failure, diffuse congestion of lungs, liver and intestines, marked diffuse alveolar oedema degeneration of centrolobular hepatocytes, increased mast cells
27
type 2 hypersensitivity - cytotoxic
antibodies react with antigens on cell surfaces or in ECM destroy target cells - trigger inflammation or interfere with normal function IgG and IgM 3 mechanisms - opsonisation and phagocytosis - IMHA inflammation - glomerular nephritis, vascular issues, organ rejection dysfunction - myasthenia gravis
28
hypersensitivity type 3 - immune complex
antigen-antibody complexes formed inflammation at site of depostion eg blue eye in canine adenovirus, FIP
29
hypersensitivity type 4 - delayed
CD4 T cell mediated organ specific disease, inflammation - activate macrophages tuberculin skin reaction
30
acute allergic reaction
local hypersensitivity type 1 cutaneous only erythema pruritus uricaria angioedema
31
generalised (systemic) reaction
mild - skin/mucosal tissue without other organ involvement moderate - involving 2 or more organ systems severe - evidence of neurological compromise moderate and severe classified as anaphylaxis
32
mast cells
innate granulocytes in connective tissue adjacent to blood vessles and lymphatics in skin and mucosa degranulate to release histamine when exposed to inciting agent and IgE
33
histamine
increased vasodilation and permeability of vessels
34
eosinophils
only in GIT, secondary lymphoid tissues, adipose tissue, thymus, mammary gland, and uterus acts with mast cells as allergic effector unit - regulate mast cells and vice versa granule content can cause tissue damage
35
self tolerance
lack of responsiveness to own antigen 4 mechanisms - central - T and B cells apoptosed T cells pushed to becoming T regs peripherally - Y and B cells become unreactive T regs locally repress immune system
36
immunoprivileged tissues
tested, brain, eye don't communicate with blood/lymph so thymus doesn't need to tell lymphocytes not to react to self leakage into tissues --> exposure to immune response --> marked and chronic response difficult to elicit immune response to antigens in these sites
37
mechanisms of autoimmunity
defective tolerance - breakdown of self tolerance mechanisms genetic increased expression of self antigens or changes to self antigens - antigens undergo structural changes - cellular stress or injury immune system not tolerant of new epitropes inflammation/infection - upregulation of costimulators on antigen presenting cells that present self antigens infectious agents present antigens that look like self antigens polyclonal b cell activation tissue injury - self antigen release that may be altered stimulates production of cytokines
38
lupus
systemic or cutaneous - lesions in multiple tissues or just skin systemic - loss of B and T cell tolerance to self antigens autoantibodies produced type 3 hypersensitivity reaction deposition of anti-antibody complexes - in glomerulus, blood vessels, skin, and joints presentations - renal disease polyarthitis hematologic disorders respiratory or neurologic dysfunction cutaneous - often nose ulcerative dermatitis, alopecia signs - fever polyarteritis glomerularnephritis mucocutaneous lesions skin lesions lymph node and spleen enlargement diagnosis - IMHA, lymphopenia, increase CD4:CD8 ratio antinuclear antibody titre - dogs
39
pemphagus
group of autoimmune skin disease immune reaction against anchoring collagens pustules, vesicles, bullae, erosions, ulcers histo - epidermal thickening, loss of adhesion between epithelial cells
40
single gene disorders
of somatic cells, germs cells, or mitochondria autosomal dominant - polycystic kidney disease autosomal recessive - lysosomal storage disease X-linked - duchenne's muscular dystrophy
41
chromosomal disorders
turner like syndrome - x monosomy horses and pigs small body, poor comformation, angular, deformities small and inactive ovaries diagnosis by karotyping
42
complex multigenic disorders
diabetes type 1 systemic lupus erythematous
43
polycystic kidney disease
persian cats and bull terriers mutated polycysin 1 or 2 gene modified cilia function and cell proliferation and migration --> renal failure PUPD low USG azotemia bilaterally enlarged or shrunken kidneys large cysts with firm pale areas (fibrosis) in between cats - also cysts in liver and pancreas
44
lysosomal storage disease
young animals lack of protein for lysosomal degeneration pathways signs depend on part of CNS affected - ataxia, head and limb tremors typically no gross lesions may see accumulated material in macrophages in blood of CSF urinalysis - gags
45
duchennes muscular dystrophy
lack of dystrophin gene muscle fibres susceptible to repeated necrosis, regeneration and fibrosis progressive muscle atrophy --> weakness in diaphragm --> impaired respiration and hiatal hernia