Immunology Exam 3 Part 1 Flashcards

1
Q

describe the barriers of the GI, lungs, and oral cavity

A

GI: simple columnar epithelium, microvilli, goblet cells
lungs: pseudostratified columnar epithelium, cilia, goblet cells
oral cavity: non-keratinized stratified squamous epithelium

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

what are the types of mucosa associated lymphoid tissues (MALTs)? are they primary or secondary lymphoid organs?

A

gut-associated
nasal associated
bronchus associated

secondary

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

describe gut associated lymphoid tissue

A

components: peyer’s patches, isolated lymphoid follicles
regional lymph nodes: mesenteric/iliac

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

describe nasal associated lymphoid tissue

A

components: tonsils, isolated lymphoid follicles
regional lymph nodes: cervical

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

describe bronchus associated lymphoid tissue

A

components: inducible in most species
regional lymph nodes: peribronchial/mediastinal

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

describe the function of M cells, goblet cells, and paneth cells in GI barrier

A

M cells facilitate transcytosis of antigens across enterocytes to present to immune cells
Goblet cells = mucins/mucous
paneth cells = antimicrobial proteins

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

most important anitbody for mucousal immunity

A

IgA

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

what is an inductive site vs an effector site

A

inductive site is a secondary lymphoid tissue where immune response is initiated (e.g. peyer’s patches (GALT), mesenteric lymph nodes, tonsils (NALT), BALT, peripheral lymph nodes)

effector sites are everywhere else (SI, LI, glands, bone marrow, cervix, inflamed non mucosal tissue)

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

what are the six types of antigen sampling methods

A
  1. paracellular transport across tight junctions
  2. apoptosis-dependent transfer
  3. antigen capture by transepithelial dendrites (TED)
  4. transcytosis (bulk & receptor mediated transport across M cells)
  5. FcRn-dependent transport
  6. uptake via goblet cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are involved in tolerance

A

anti-inflam cytokines like IL10 and TGF-beta
innate lymphocyte cells
Treg lymphocytes
IgA producing B cells
fibroblasts

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

what are involved in inflammation

A

proinflam cytoines like IL6 and IL1-beta
Th1, Th2, Th17

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

how is IgA transported to mucosal surfaces

A
  1. IgA J-chain binds to plgR on basolateral face of epithelial cell
  2. endocytosis of IgA
  3. transcytosis of IgA to apical face of epithelial cell
  4. release of IgA dimer at apical face
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are IgA effector mechanisms

A

-bind/neutralize pathogens/toxins on gut surface or internalized in endosomes
-export toxins/pathogens to apical surface while being secreted
-bind to Dectin-1 on M cell to allow transport of antigen to dendritic cell or any APC

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

describe the difference in serum IgA and mucosal IgA

A

serum IgA = pentamer
mucosal IgA = dimer

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

what are intraepithelial lymphocytes (IELs)? what are there effector mechanisms?

A

CD8+ cytotoxic T cells in the epithelial lining of the gut

  • once virus infected mucousal epithelial cell, IELs will kill infected epithelial cell via perforin/granzymes and Fas-dependent pathways (apoptosis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

list the main effector mechanisms of mucosal immunity

A

memory T cells
natural effector/regulatory cells
mucins/mucous
IgA
antimicrobial peptides (AMPs)
distinctive microbiota

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

what is the difference between a mucosal and parenteral vaccine

A

parenteral - given elsewhere in the body other than mouth or alimentary canal, mainly systemic immunity
mucosal - given mouth/nasal cavity/alimentary canal; mucosal and systemic immunity

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

where do B cell originate in avians compared to mammals

A

Bursa not Bone Marrow

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

do birds have lymph nodes?

A

no lymph nodes, but build lymph node aggregates in areas of infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what immunoglobulins do avians have

A

IgM, IgY, IgA
do NOT have IgD or IgE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

how does the IgY chain in avians differ from IgG in mammals

A

IgY H-chain is longer, 5 domains, and no hinge region

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what are heterophils?

A

avian equivalent to neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what are the differences in thrombocytes between mammals and avians

A

avian thrombocytes are phagocytic (reason why you do not what to drain abcesses)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

do avian species have a simpler or more complex immune system? why?

A

simpler
lay eggs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

how are the bursa in avians and thymus in mammals similar

A

both regress with sexual maturity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

describe the difference in avian MHC complexes

A

minimal essential MHC
only 2 class I genes & 2 class IIbeta
usually only one is expressed making it harder to fight off intracellular pathogens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

how to avian species generate antibodies compared to mammals

A

gene conversion

random recombination of pseudogene V sequences and rearranged sequences occur within bursa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what are avians primary lymphoid organs and function

A

Bursa - B cell production
Thymus - T cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what are avian secondary lymphoid organs

A

spleen
harderian gland
cecal tonsils
peyer’s patches
meckel’s diverticulum
other (islet of lymphoid tissue or microbiota)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

function of the harderian gland

A

IgA producing plasma cells, also some IgM and IgY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

why is the spleen more critical in avians than mammals

A

site of progenitor B cell lymphopoiesis
site of interaction between lymphoid and nonlymphoid cells so due to avians lack of lymphatics, spleen is more critical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

function of cecal tonsils

A

B and T cell production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

function of peyer’s patches

A

B and T cell production

34
Q

function of meckle’s diverticulum. what is it?

A

role unclear
remnant of yolk sac found 1/2way down small intestine
IgM producing B cells 2 weeks post hatch
IgA and IgY producing B/T cells 2-4 months post hatch

35
Q

what is meant by seasonality?
what factors influence this?

A

energy-expensive processes (e.g. immune system) need to be timed appropriately to maximize fitness

factors: photoperiod, food, weather, temp, reproduction, growth, molting, migration, change in disease/parasite pressure

36
Q

describe the immunity of invertebrates

A

rely exclusively on innate immune mechanism

37
Q

describe invertebrates physical barriers

A

chitinous exoskeleton
antibacterial proteins
mucus

38
Q

what are the 6 types of invertebrates innate immune defenses

A

phagocytosis
cytokines
protease cascade (melanin - wound healing)
TLR & other PRR
antimicrobial peptides (defensins, lectins, lysozymes)
RNA interference

39
Q

how does invertebrate phagocytosis differ from mammals

A
  • hemocytes and coelomyocytes as phagocytic cells rather than dendritic cells, macrophages, etc.
    -cytokine-like (e.g. IL-1-like) molecules that activate phagocytic cells & promote phagocytosis
40
Q

how do we know invertebrates have cytokine-like molecules

A

LPS stimulation of mollusk hemocytes resulted in the release of other mediators

41
Q

function of Melanin in invertbrates

A

antibacterial properties (antimicrobial activity, wound healing, pigmentation)

42
Q

what is Spatzle?

how does this differ from mammals?

A

protein ligand that indirectly activates TLR after pathogen recognition via PAMPS

mammals use direct recognition of pathogens with PAMPS

43
Q

what is the dicer enzyme

A

degrades dsRNA into small fragments so they can bind to RISC complex

aids in the RNA interference mechanism to prevent viruses from replicating within infected cells

44
Q

what adaptive immunity does an invertebrate have

A

Ig-like molecules, such as Dscam (down syndrome cell adhesion molecule) which has similar structure/function to Ab
- opsonization = enhances phagocytosis by hemocytes

45
Q

what are the first vertebrates to utilize adaptive immune system

A

jawed fish

46
Q

how do cyclostomes (jawless) immunity differ from mammals

innate?

adaptive?

A

innate
-antimicrobial proteins and complement factors
-monocyte-like cells & lymphocyte-like cells
adaptive
no recombination for antibodies or TCR, so they synthesize variable lymphocyte receptors (VLRs) by gene conversion (similar to birds) rather than Ab or TCR
(VLRA, VLRB, VLRC similar to mammalian TCR and BCR adaptive immunity)

47
Q

describe jawed fish innate immunity

A

toll like receptors (TLR)
granulocytes, macrophages, lymphocytes, NK cells
lysozymes, lectins, defensins, APP, complement, eicosanoids, cytokines, chemokines

48
Q

describe differences between jawed fish and mammalian immunity

A

NO bone marrow or lymph nodes
less diverse gene arrangement due to less gene segments
predominantly IgM (variable structures in diff species)

49
Q

describe jawed fish adaptive (humoral) response

what cells does the thymus, kidney and spleen make

A

rely on complement mediated lysis, no opsonization
antibodies found in most tissues including egg yolk
response is seasonally dependent and affected by social interactions (similar to birds)
Thymus makes T cells
Kidney makes B cells
Spleen makes B
intestinal lymphoid tissue (hindgut) makes B cells
RAG recombinase for gene rearrangment
MHC I and II

50
Q

why is graft rejection lower in cartilaginous fish than mammals

A

they have less diversity in their gene segments

51
Q

describe key components of amphibian immune system

A

antimicorbiral peptides in skin
complement most efficient at low temps
Ab & TCR gene rearrangment
complex changes associated with individual growth impact immune development/function

52
Q

urodele immune system

A

no bone marrow
do have thymus = T cells
kidney = B cells
red/white pulp not separate in spleen = B cells
monomeric IgM
slow graft rejection
memory at least 90 days

53
Q

anuran immune system

A

bone marrow = B cells
thymus = T cells
lymphnode-like structures
circulating T and B cells
IgM
NK cells & cytotoxic-T cell-like
IgM and IgY most important (5 isotypes)
functional T cell receptors
MHC I and II

54
Q

monotreme immune system

A

antimicrobial peptides/complement
gene rearrangment
spleen, thymus, GALT
NO lymph nodes, but do have lymphoid nodules
IgG predominates (8 isotypes)
unique IgO

55
Q

marsupials immune system

what is unique about the opossum

A

antimicrobial peptides/complement
gene rearrangment

4 isotypes (IgM, IgG, IgE, IgA)

opossum has early 𝝁TCR chain expressed early provide protection during first few days of life

56
Q

first species to produce IgG

A

monotremes

57
Q

what is the purpose of fevers?

how do ectotherms achieve this?

A

vertebrates respond to antigens fast and more intensely at high temps

ectotherms “heat seek” because they are immunosuppressed/helper T cells sensitive at low temps

58
Q

how does hibernation affect the immune system

A

hibernation = immunosuppressed

metabolic depression “torpor” when the body temp drops can affect blood leukocyte #, complement levels, phagocytosis, cytokine production, T cell proliferation and antibody synthesis

fasting can also affect immune function

59
Q

Describe differences between the uterine environment and the environment an animal encounters after birth

A

Uterine environments are sterile whereas the environment an animal encounters after birth has increased risk of pathogens, but those help develop immunity

60
Q

Compare times of gestation, development of lymphoid organs, and circulation of blood lymphocytes in different species

A

foals have the longest gestation, time for lymphoid organs to develop and time for blood lymphocytes to circulate, then calves, then puppies

61
Q

List important components of the innate immune system of newborns

A

antimicrobial molecules (defensins, lactoferrin, surfactant proteins, lysozyme)
TLR
NK cells
neutrophils (weaker)
macrophages (gradually become better)
commensal organisms

62
Q

Theorize why a Th2 response is favored in mammalian mothers during pregnancy

A

reduce risk for fetal rejections

Th2
- IL-4,5 for parasitic pathogens
- activates eosinophils and B cell switch to IgE or IgA
- dampens IFN-gamma
- immunosuppresses Th1 for less inflammatory responses which protects fetus from rejections

63
Q

Diagram differences in four types of placenta and indicate how this affects transfer of antibodies to the fetus

A
  1. hemochorial placenta: humans/primates, maternal IgG direct transfer
  2. endotheliochorial placenta: dogs/cats, 5-10% of IgG direct transfer
  3. epitheliochorial placenta: horses/pigs, no transfer of Ig across placenta, dependent on colostrum
  4. synepitheliochorial placenta: ruminants, no transfer of Ig across placenta, dependent on colostrum
64
Q

what is passive immunity

A

immune support from mother (antibodies, complement, lymphocytes) passed through placenta or colostrum

absorption of IgG protects against neonatal septicemia

65
Q

Indicate how intestinal microflora effect functions of immune system

A

exposure to complex mix of PAMPS
DC present microbial antigen to CD4+ T cells
balance Th1 vs Th2

66
Q

Describe differences in the neonate intestine that allow for absorption of colostrum

A

low protease activity
open gut for 6-8 hours postpartum
specialized enterocytes with FcRn receptors on brush border - bind Ig and transport them

67
Q

when is permeability of enterocytes maximized for colostrum absorption

A

6-8 hours after birth, declines rapidly at 24 hours when specialized enterocytes are replaced by mature cells that increase digestion of proteins not absorption

68
Q

List nutritional and immune components of colostrum

A

electrolytes, carbs, fats, proteins (80% protein = Ig)
IgG and IgA
complement
pro-inflam cytokines
lymphocytes
trypsin inhibitors

69
Q

Define failure of passive transfer.
What is a common sign of failure of passive transfer?
what can this lead to?

A

failure of Ab to be passed to neonates
no protein in urine or serum
leads to infection

70
Q

what maternal factors lead to failure of passive transfer?

A

colostrum quality
poor mothering
loss of colostrum before birth
poor health
parity (more than one offspring)
low pathogen exposure

71
Q

what neonatal factors lead to failure of passive transfer?

A

premature birth
health of intestine (improper GI development)
failure to nurse

72
Q

predominant Ig in cattle colostrum

A

IgG

73
Q

predominant Ig in horses and pigs colostrum

A

IgG

74
Q

predominant Ig in dogs colostrum

A

IgA

75
Q

predominant Ig in cats colostrum

A

IgG

76
Q

predominant Ig in primates colostrum

A

IgA

77
Q

Know how to determine if a neonate has received adequate colostrum

A
  1. proteinuria - protein in urine due to immature glomerulus
  2. serum IgG assessment 18-24 hours after birth
    - foals >800 adequate
    - calves total protein 5.8-6.3 ideal
78
Q

Indicate how to treat failure of passive transfer in neonates < 24 h old as compared to neonates > 24 h of age.

A

< 24hours - before gut closure, tubing w/ colostrum

> 24 hours - after gut closure, IV plasma administration

79
Q

Discuss how maternal antibodies protect neonates and interfere with vaccination of neonates

A

protect neonates via transfer of IgA and IgG

can suppress neonates immune response and cause disease = infections or alloimmune conditions (autoimmune diseases)

interfere with vaccination of neonates because maternal Ab last 4-6 months (horses) and about 8 weeks (dogs) and will neutralize Ag and inhibit B cell response by masking Ag

80
Q

in what order does immune cell development occur in the fetus

A

thymus first
then spleen, lymphnodes and bone marrow

81
Q

what would high IgG at birth indicate

A

intrauterine infection

82
Q

what is the importance of mucosal epithelial cells in mucosal immunity

A

turnover frequently
uptake nutrients
TLR & NOD receptors which stimulate production of antimicrobial peptides & proinflam cytokines