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Host Defense > Final Exam > Flashcards

Final Exam Flashcards

1
Q

What is the primary function of the innate immune system? Name the 7 innate immune cells. What 2 cells are shared with innate and adaptive?

A

Making a barrier.
macrophages, neutrophils, mast cells, eosinophils, basophils, NK cells, dendritic cells
NK T cells and delta gamma T cells.

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2
Q

Function of neutrophils?

Most important phag cell? Has what receps/ Secretes what?

A

phag and digest of bact and particles
Macrophages
fc and complement receptors
pro inflamm cytokines

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3
Q

What kind of receps do eosinophils have?
Mast cells are loaded with what on their surface? What receptors (parasites.
Surface IgE crosslinks when? Degrans toxic/proinflamm products.

A

Fc receps for IgE.
IgE.
FceRI
Ag binds.

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4
Q

What is the most important APC? Why?

What are the 3 main phagocytes?

A

Dendritic cells- connection between innate and adaptive immunity.
Macrophages, dendritics cells, neutrophils

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5
Q

After phagocytosis, phagosome fuses with what? Contains granules. What acidifies>
What cell generates an oxidative burst, which releases what?
Do avian macrophages make a lot of ROS?

A

Lysosome.
NADPH oxidase.
Neutrophils (macrophages a little), toxic oxygen byprods

NO

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6
Q

Acidification of the phagasome triggers what enzyme activity? What 5 ROS are created in teh cascade?
Species dependent macrophages make what oxide in the cascade?

A

Respiratory burst (synth of ROS).
Superoxide anion, hydrogen peroxide, oxygen singlet, hydroxyl radical, hypochlorite.
Nitric oxide.

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7
Q

ROP attack what in bacteria? Nitric oxide species attack what? Both damage what of the bacteria?

A

Metal centers of the bacterial enzymes.
Repiratory chain
DNA.

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8
Q

NK Cells are of what lineage. Are generally in primary or secondary lymph organs? Possess which receptors?

A

Lymphoid
Secondary
Fc

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9
Q

Are NK cells antigen specific/MHC specific?
Produce what cytokines?
Stim by what molecules favor effector function (cell killing) and what molecule favors cytokine secretion?

A

NO NO
IFN gamma and TNF alpha
IFN alpha and beta favor effector function.
IL 12 favors cytokines.

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10
Q

Nk cells and Tc cells both recognize their targets via what? but what is diff about NK cells? How is it inhibited?

A 
MHC class 1 molecules. LACK of molecules activates NK cell. 
Killer inhibitory receptor (KIR) trasmitted if MHC class 1 bound.
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11
Q

NK cells also have receptors for what that are usually found on cells after infection, trauma, stress.
Therefore, NK cells are activated depending on a balance of signals.

A

Carb ligands (MIC A, MIC B).

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12
Q

NK cells hav Fc receptors involved in a process called what? What does this mean? Kills like CTLs-how?

A

ADCC-Antibody dependant cell mediated cytotoxicity= CD16 Fc receptor
Antibody bound to the target cell surface due to an antigen. Fc portion of the immunoglob is recog by Nk cells. Killed by perforin release.

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13
Q

Innate-LIKE lymphocyte is called what? Clonal expansion? Antigen specific? Produce cytokines? Associated with CD?? Less V segments. Dont interact with APCs due to lack of what molecules? Fight against what? Also function in what? Located where? May recirc.

A 
gamma delta T cell.  NO
Yes
Yes
CD3.       CD4 and CD8
Microbial invader. Wound healing. Skin and intestinal epi.
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14
Q

Name the 5 main antimicrobial peptides in innate immunity with the 2 main categories first.
These peptides are small and cationic. Made by two cell groups.
Epi alpha and beta defensins form what? (alpha and beta only differ by how cysteines link together).
Cathelicidins form what?

A

cathelicidins, defensins, lactoferin, histatins, lysozymes
PMNs and epithelial cells.
beta pleated sheetst
amphipathic alpha helices.

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15
Q

Antimicrob peptides are anti-viral, parasitic, fungal and bact. Constitutive and induced. Chemotact and stim immunocytes.
How are defensins attracted to microbial membranes? Do what?

A

electrostatically attracted to cholesterol free negative charged membrane. (is positive).
Fxn: forms ion channel, forms pore, distorts bilayer.

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16
Q

How many types of defensins exist? Depends on what? Theta defensins are circ. not in? 3 cell types that release defensins? Is expression of defensins inducible? Highly divergent between tissues and species.

A
  1. How cysteines link. Not in humans or new world primates.
    Epi (paneth cells), macrophages, neutrophils
    Yes!
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17
Q

What defensin is released by paneth cells and leukocytes? Phagocytes release defensins into what? Male repro releases what defensin?

A

Alpha, into phagolysosome, beta.

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18
Q

defensins stim 2 cells ESPECIALLY memory t cells that do what? Also mast cell degran, dendritic maturation.

A

innate immune cell and T cell chemotaxis.

Esp memory Ts that use CCR6 o bind beta defensin 1.

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19
Q

Cathelicidins toxic to what? Chemotactic for 2. Released by? Are pathogens getting ressitant strategies to this or defensins?

A

bact and fungus. mast cells and neutrophils
Neutrophils.
BOTH.

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20
Q

What kind of deficiency is related to infection due to low cathelicidin and defensins? Therefore altered defensin gene expression is associated with?
Both cathelicidins and defensins are expressed where?

A

Vit D
Skin Dz.
Sites of environemental contact.

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21
Q

Lysozyme protects against what? Cleaves bond between what 2 acids in the cell wall of a bacteria. What does this do? Lysozyme is expressed where? High in human milk. Released by what 2 cells.

A

bacterial infection.
Bond between NacGlu and NAM in cell wall.
This breaks the cell wall and the bacteria burst under their own pressure.
On most mucosal membranes and within endosomes. Neutrophils and macrophages.

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22
Q

Lactoferrin is found in what? Main fxn? Very im in neonatal immunity of the gut. Released by what cells?

A

Found in milk and other mucosal secretions. Main fxn is to bind iron and taken away from bacteria.
Released by epi cells and neutrophils.

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23
Q

Histatins are released from what? these are rich in histidine and fucks the lipids of what?

A

salivary glands. Fungal lipids.

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24
Q

What are the responses of the T and B cells of the adaptive immunity against bacteria?

A

B-neutralization, opsonization, pha of c3b bact, inflamm, bacterial lysis
T cells-antibody response, macrophage activation, inflamm

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25
Q

Name the 4 main non specific branches of the innate system against bact and what they do?

A

phags-phag
NK cells-lyse
cytokines-inflamm and macrophage activation
complement-lysis, inflamm, phag

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26
Q

What kind of bact is there NONE of vet significance. Cell surface is made of 2 things. DOes gram + or - have a thicker peptidoglycan layer? Which has the LPS

A

?gram neg cocci. Cyto membrane. Cell wall.

Gram + has thicker peptidoglycan. LPS is in gram -

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27
Q

What are the two polysaccs that make up peptidoglycan? What are techoic acids and where are they found?

A

Nacetylglucosamine and N acetylmuramic acid.

Repeated crosslinked simple sugars (can be highly antigenic) in gram +cell walls.

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28
Q

What are the 3 portions of LPS?

Name the 3 non essential bacterial appendages and describe.

A

O antigen, core and Lipid A.

  1. ) flagellae-non brownian locomotion-glycoproteins(antigenic)
  2. ) fimbriae-smaller, more on cell. Not motility, attachment to host cells.
  3. ) capsule-slime covering, can mess up phag, lysis, attachment, desiccation, etfc
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29
Q

Summarize kochs postulates.

What are the 3 basic processes to prevent bact colonization?

A

get microorg from dead animal-id-grow-inject into healthy mouse-cause dz-id-grow.
surface barrier, innate and adaptive immunity

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30
Q

Name some non spec and spec surface defenses

A

non spec-skin, flora, low ph, flushing action, lysozyme, defensins, lactoferine, phagocytes, complement.
Spec-sIgA, Abs, Tc

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31
Q 
Some bacteria (2 ex?) evade the barrier function all together. How? 
Enteric pathogens like what? Can indirectly or directly disrupt what which compromises the epi cell barrier.
A

Shigella/ listeria. leave vacuole. access cyto-exist in infected cells
E Coli- tight junctions

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32
Q

Other antibact: complement, antimicrobial peptides. What proteins are produced by bact which bind Fe2+ to compete with host?
When phags lysosomes fuse with phagosomes, what 5 things happen?

A

Siderophores.

acidify, ox burst, release cationic peptides/defensins, release proteases, activate competitors like ferritin

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33
Q

Phags bear MANY receps. In the process of making ROP, nitric oxide is made through a sep cascade by what enzyme?
Phagolysosome properties are 2 categories.

A

nitric oxide synthetase.

oxidative or non oxidative.

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34
Q

Bact have 3 general ways of evading intracell destruction. How are they antioxidant?

A

escape into cyto, prevent lysosome/phag fusion, resist lysosomal enz
Can deactivate products by making their own catalase or superoxide dismutase.

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35
Q

How do neutrophils kill extracellularly?

A

NETs (neutrophil extracellular traps) made of DNA and histones covered in antimicrobial proteins and released and ensnare microbes. Neutrophil death. Requires ROS. Pro inflamm

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36
Q

Acute phase proteins released from what? due to what signals? Name some and what they cause?

A

Liver, due to LPS, TNF alpha, IL6.

Some are SAP, CRP, MBL, fibrinogen. Cause opsonization, complement

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37
Q

Danger signals are released by cells that are undergoing cell damage. Loss of what from cyto causes dimerization of what which releases what?

A

K+ efflux causes NALP dimerization which allows local pro inflamm signals.

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38
Q

What has recently been found that can recognize evolutionarily conserved structures and patterns on diff pathogens.
What ligands to TLR 2/6, 3, 4, and 9 react to?

A 
Toll like receptors (TLRs). 
2/6 gram positive and fungi
3-Double stranded RNA
4- gram - (LPS)
9-DNA with unmethylated CpG
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39
Q

How well do TLRs recognize microbes? Inner/endosome or outer membrane for 2/6, 3, 4, 9
TLR signals are REQUIRED for what activatioN?

A

PERFECTLY.
2/6-outer 3-inner 4-outer 9 inner
Phagocyte

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40
Q

1st response to TLR is to make what? Overlapping cascades of kinase reactions, but the most important is what transcription factor which does what? TLR3 activates what gene? TLR 7?

A 
make cytokines. 
NF-kB
activates cytokine genes and how strongly they are expressed. 
IFN beta
IFN alpha and beta
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41
Q

More TLRs are recruited to phagasomes when?

How do TLRs provoke a specific adaptive immune response?

A

During an infection.

Different cytokines are released, causing specific adaptive immune response. –OTHER LINK BETWEEN adaptive and innate

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42
Q

what are NODs? Activate what gene? Work with TLRs?

A

Nucleotide binding oligomerization domain proteins. More ancient than TLRs, detect PAMPs in cytoplasm, since TLRs cant.
Activate NF-kB as well
WOrk together

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43
Q

ANTIVIRAL-What is the innate immune response of protection against a viral infection? Adaptive? Both for eradication of an established infection?

Other innate immunity processes?

A

Innate-antiviral state of cell via interfeurons
Adaptive-antibody neutralization.
Innate-NK cell killing
Adaptive-Cytox t cell APCs via MHC class 1.

complement, interferons, NK cells, cytokines, chemokines, defensins

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44
Q

Tc cells are activated by MHC class 1. Th augment Tc cell via what secretion. What do Tc cells secrete to block viral rep.

What 4 cytolytic granules are released by Tc cells on viral infection. Lysis of infected cell-not always the answer!

A

IL 2
IFN gamma
–perforin-pore on cell, allows granzyme in
–granzymes-proteases, cleave proteins on cell membrane
–granulysin-induces apoptosis
–lymphotoxin-induces cell death via apoptosis.

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45
Q

BUT viruses can block MHC class 1 to escape immune response. give 3 ex

A
  • -prevent peptide movement through TAP transporter.
  • -prevents peptide loading onto MHC class 1 proteins
  • -dislocate MHC 1 molecules into cyto for degradation.
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46
Q

Some viruses interfere with apoptosis. Other than blocking MHC, explain other ways.

A

Prevent caspace, induce anti apoptotic genes, inact granzymes, prof virokines, inhib Tc fxn.

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47
Q

Once a virus in intracell, antibodies cannot directly reach it. What is ADCC? Is lysis always the primary function of NK cells?

A

Antibody dependent cellular cytotox-Antibody binds to cell, recruits NK cells and macrophages to kill the cell
No.–may be secretion of cytokines (ifn alpha/beta and TNF alpha)

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48
Q

What are 5 general categories of how a virus can evade NK cells

A

1.) viral MHC class 1 homologues (MHC1 inhibits NK cells) 2.) Increased gene expression of inhibitory protein 3.) Decrease activating ligands or increase antagonist 4.) Bind up activating cytokines, make cytokine homologs, increase host prod of inhib cytokines. 5.) Direct infection.

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49
Q

What 3 things do antibodies do to virally infected cells (humoral)

A

neutralization, opsonization, complement

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50
Q

Viruses can evade antibody immunity via direct or indirect antigenic shift. Define.
How can a capsid be affected to cause evasion by a virus?

A

Genomic re-assoirtment for viruses that have segmented genomes.
Shed antigen from capsid proteins or include viral proteins in the capsid to block complement.

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51
Q

Completemt has what effect on CV? Why imp?

How do viruses inhibit complement?

A

Pro inflamm=increase permeability–IgG, IgM, Tc cells can come in.
Many diff viruses can effect many diff steps.

52
Q

Most important thing in innate immunity is what secretion? Most important one?
When Interferon 1 is bound to a receptor, it enters a what state? Name the two enzyme that are released and what they do?

A

Cytokines
Type 1 interferons
Antiviral state
2’5’-OAS-makes polymers of 2’5’ Oligo A, activated RNase L which cause mRNA degradation.
PKR- this protein kinase stops phosphorylation initiation factor 2 (an elongation factor for the translation of proteins) Inhibs protein synth.

53
Q

Why dont 2’5’ OAS and PKR affect human cells?

Type 1 Interferons also induce what proteins which has an unknown fxn that causes what? Usually 2 genes. Why?

A

Euk has a 5’ cap. PKR does a little (decrease prot synth)
Mx proteins—causes an interferance in replication of RNA viruses.
One in cyto and one in nucleus (because viruses replicate in both)

54
Q

Both induced by type 1 interferons: What do APOBECs do ?

What about ADARs?

A

APOBECs removes an amine group from cytosine residues in DNA. Purposeful mutation. C/G–> T/A
ADARS remove amine groups from adenosines in RNA. A/T–> C/G

Net effect: codon changes

55
Q

APOBECs hitchhike where? What happens?

PAMPs like 2 are also used as antiviral immunity. Trigger what transcription.

A

Within the virion. Mutations until replication is impeded.

TLR-3 and NOD. IFN alpha and beta through NF-kB

56
Q

Parasites kill more people than fungal, bact and viral. Induce what kind of inf.
Adaptive imm against them. Antibodies that what to trigger complement?
What antibody binds to mast cells/eosin=degranulation?

A

Chronic.
Opsonization
IgE

57
Q

Parasites tend to evoke a very polarized Th1/Th2 response. Which is better? Why?
Why is crypto. parvum so hard to have a response to? What takes care of it?

A

Th2. Less inflamm.
Encysts on the animal intestinal epi. Takes nutrients from cells. IgE, mast cells and NK cant get to it. So, gamma delta T cells must sense the “stressed” cell.

58
Q

Define vaccination and immunization

A

Vacc-deliberately giving an antigen to elicit an immue response
Immunization-providing the body with defense against an antigen. Broader- Vacc and other processes

59
Q

Define passive immunzation. How long does this last? 2 probles?

A

protection of one ind. transferred via Ab, B or T cells from another ind.
Usually short lived with no memory
Can induce hypersens and can transfer other infectious agents.

60
Q

Define natural and artificial passive imm

A

Natural-passed from mother to fetus/neonate via placenta or colostrum
artificial-Abs from one ind are given to another.

61
Q

What is another name for active immunization? How long does it last? Can boost.
Name the 3 types of vaccinations and give ex

A

A vaccination.
Prolonged=memory.

Whole organisms-killed/inactivated, attenuated live
Subunit/component-toxoid
DNA vacc

62
Q

Killed/inactivated vaccs mostly only induce what? Generally no memory. How much antigen? How long is protection? What is required? 2 advantages? Generally what is added? How are they inactivated?

A 
Antibodies
Large amounts
Shorts
Boosters
--stable, unlikely to cause dz
Adjuvant
Must maintain antigenic integrity. Can heat treat=denatures. Chemical is common, but must remove to avoid tox. Can inat live but unable to replicate.
63
Q

Live vacc induce what responses? Causes what but not dz. How is this made?

A

Th1, Th2, CTL.
Infection
Grow in vitro until virulence is lost. Also, rDNA can be used to directly mutate or remove the virulence gene.

64
Q

What is a subunit vacc? Component/conjugate?

What is the big disadvantage?

A

Subunit-only defined proteins.
Antigen is complexed with carrier prot=increased immunogenicity.
Disadv-only stims immune against that single prot. Must carefully choose antigen.

65
Q

Toxoid vaccines- how do they work? How are they made?

A

For pathogens which a secreted toxin is the cause of dz or illness-target just the toxin. Made by treating toxins with chemical or by heat.

66
Q

How do DNA vaccs work?

Marker vaccines are also called?

A

Plasmids with the genetic info of the antigen is injected ito muscle cells. MHC 1 and cell mediated immunity causes prod of the encoded protein.
DIVAs-differentiate infected from vaccinated animals

67
Q

DIVAs have one of 2 things.

A

An additional protein not found in the path or missing a protein not essential for the path to grow, but recognized by the immune system.

68
Q

Adjuvants-define. Work in 3 ways.

A

enhance immunogenecity of an antigen. Most proteins are degraded quickly and low B and T cells. This keeps protein there longer with a stronger immune response.

convert soluble proteins to particulate
stim cytokine prod by APC
Depot effect to maintain Ag half life.

69
Q

Disadv of injectable vacc?

A

–cost of needles–very artificial entry for path–typically induce primarily igG response. –most path are encountered on mucosal surface.

70
Q

3 cell types most involved in Tumor cell destruction?

A

NK cell, T cell, macrophages.

71
Q

What are the 3 branches of immunotherapy for cancer? GOal of non specific?

A

non-specific, active immune stimulation and passive stimulation

engage the innate and adaptive arms of the immune system to recognize and attack neoplastic cells.
Engage the innate and adaptive immune system to attack neoplastic cells.

72
Q

non specific: Iv injection of liposome encapsulated muramyl tripeptide increases serum levels of what 2 things?

A

TNF alpha and IL 6 (derived from mycobact wall)

73
Q

non specific: Cytokine therapy: use what cytokines? IL 2-Activates what? Side effects? How to minimize?

A

IL 2, IL 12, TNF alpha- activates T cells, stims APCs, enhances NK and LAK cell fxn.

Side effects: caillary leakage, hepatocellular necrosis, renal tox
min by localized therapy, disguise IL2 to deliver to tissue, use lower doses.

74
Q

IL 12 increases what 2 things? Enhances what cel? Severe side effects in humans. Targetted approach may work.

A

IFN gamme and tnf alpha from NK and T cells. Enhances dendritic cell activity.

75
Q

Tumor necrosis factor alpha: produced by? Stims what cells. Cytotoxic. Very potent inflamm. Key mediator in what dz. What happens when it is PEG-ylated.

A

dendritic cells. T cells, Septic shock.

evades recog by immune system, prolonged half life, lowers tox, increases response.

76
Q

PASSIVE stimulation: hybridomas Bcells producing waht? What did they do to mice?

A

antibodies. Humanize by injection human genes and desired antigens.

77
Q

Passive: 8 Mabs for cancer: Rituximab highly expressed where? Bevacizumab: anti vegf. What is vegf.

A

Surface of human B cell lymphoma.

Used to revasc by tumor.

78
Q

Active: vaccines: what cancer vaccs are in the works in vet med?
What is the enzyme responsible for melanogensis?

A

Gliomas, equine sarcoids, canine papilloma, canine malignant melanoma
Tyrosinase (in vacc)

79
Q

Spontaneous remissions with some cancers in vet med. What is a Sx for osteosarcs that are said to increase life expectancy. Infection with implant might do what?

WHAT TX CURES MORE CANCERS TAHN ANY OTHER?

A

Limb sparing sx. Increase life.

SX

80
Q

Today: coley’s toxins? what are they?

A

Anaerobic bact have affinity for hypoxic tumors=alter LPS. 25% success.

81
Q

Tumor definition? What is a new growth occuring in excessive and unregulated manner? Two type ?

A

Swelling
Neoplasm
Malignant-invades the tissues around via circ or lymphatics.
Benign-noninvasive

82
Q

Cancers arise from any tissue cell. Name the 4 categories and desc

A

Sarcoma-mesenchymal tissue-fibroblasts, muscle, fat carcinoma-epi lymphoma-lymphocytes leukemia-blood or bone marrow leukocytes.

83
Q

What are the 3 steps of cancer development and describe.

A
  1. ) tumor initiation: unrepaired alterations in cell DNA (chemical or physical) or genetic mutations in cell DNA. Preneoplastics cells
  2. ) Tumor promotion: neoplastic cell growth, agents that cause mitogenesis can be promoters.
  3. ) tumor progression: invasive growth.
84
Q

Name 7 characteristics of cancer cells

A

-stim own growth–ignore growth inhib signals–avoid apoptosis–own blood supp (angiogen)–metastasis–replicate continuously–evade or outrun the immune system

85
Q

Name 5 ways tumors escape immune recog.

A

low immunogenicity, treated as self antigen, antigenic modulation, tumor induced immune supp, tumor induced privelaged site.

86
Q

Tumor antigens can be split into 2 groups;

1st is derived from what, so results in what?

A

tumor specific antigens and tumor associated antigens
mutated, silent or viral genes expressed by tumor cells. Results in presentation of foreign antigen by MHC. T cell and antibody response,

87
Q

Products of mutated genes: what is an oncogene? a protooncogene?

A

oncogene: gene that when dysregulated, its protein prod participates in the onset and development of cancer
proto: normal gene that becomes an oncogene with mutations or increased expression. Help cell growth adn diff.

88
Q

What are tumor associated antigens? What are oncofetal antigens? Altered glycosylation?

A

Normal cellular antigens that are expressed atypically. Less efficient at invoking an immune response since they arent perceived as foreign.

  • -proteins present only during fetal dev that are found in adult cancers.
  • -cell surface lipids and proteins can have altered glycosylation can occur by the abnormal addition of glycan structures to cell surface proteins and lipids
89
Q

What are the 5 main immunosurveillance cells?

A

cytotoxic t lymphs, helper t lymphs, macrophages/neutrophils, b cells, Nk cells.

90
Q

sim and diff between Nk cells and cd8

A 
sim-both cytotox, recognize class 1MHC
diff-dont have t cell recap and kill if no MHC1
91
Q

What are the 3 standard therapies for tumors.

What are the two categories for immunotherapies

A

surgery, chemo, radioation

active therapies and passive therapies

92
Q

Active therapiesL augmentation and vaccination. describe

A

–nonspecifically stim the immune system. Acemannan and mycobact bovis-complex carbs or bact, induce macrophages to secrete pro inflamm. Tx fibrosarc
Vacc-response against tumor antigens

93
Q

Passive therapies: explain leucocyte adoptive transfer and anti tumor Abs

A
  • -leukocytes from the patient are expanded in the lab and reinjected.
  • -admin Ab specific for tumor antigens (ADCC).. atibodies can bind and stim NK cells, antibody toxin complexes bind, antibody radioactive complexes bind.
94
Q

Passive immunity from mother to newborn is in 2 steps.

Name the three placentas, specieis and describe transfer of Ab

A

trasnfer of maternal Abs in the blood to the fetus
transfer of maternal Abs in the colostrum and milk to the newborn
1.) hemochorial-maternal blood in direct contact with placenta. IgG transferred to equial levels. humans and primates.
2.) endotheliochorial-endo of maternal caps with placenta. cats and dogs. 5-10% of maternal antibodies
3.) epitheliochorial-placental epi in contact with uterine tissue. NO TRANSFER. Horses and ruminants.

95
Q

Colostrum contains 5 things

Ab in milk are from 2 places

A

proteins from blood, cytokines to promote immune, IgG, IgA, IgM

blood and local B cells in mamm glands

96
Q

what is low initially in a new born GI to keep Ab from degradation?
Immunoglobs from milk and colostrum are brought into circ how?
Maternal immunoglob protection goes from what to what in the newborn.

A

Protease.
Fc receps on epi of GI.
Systemic to intestinal

97
Q

Define anti idiotypic and idiotypic antibodies.

A

Mothers anti idiotypic Ab is transfered to baby after binding to an idiotype. In newborn, an anti anti idiotype binds, which is equiv to the idiotype.

98
Q

LYMPHOCYTE TRAFFICKING-continously migrate from where to where? Name the primary lymph organs, 2ndary? Lymphoid compartments are at portals of what entry? Name 4

A 
blood to tissue to do job. 
bone marrow, thymus
lymph node, peyers patch
antigen
spleen, GALT, BALT, SALT
99
Q

Lymphcytes enter lymph nodes by two routes

Explain the route of lymphatic fluid from tissues.

A

BVs and afferent lymphatics.

Tissues to 2ndary lymph organs and eventually to thoracic duct and back to blood.

100
Q

What do naive lymphs do? What are effector lymphs and what do they do?
How is lymphocyte trafficking able to happen? What if antigen recognition/clonal expansion occurs?

A

constantly migrate through all of the 2ndary organs.
T and B cells that have already differentiated from naive upon stim by specific antigen.
Capable of entering sites of infalmm and recirculate in a selective manner with preference for the 1st place antigen was encounteredd.
Regulated by adhesion molecules and chemokines.
Can change adhesion molecules and chemokine receptors they express

101
Q

Define hypersensitivity. Define autoimmunity. Type 1-3 are what mediated. 4 is what mediated?

A

–immune response occurs in excessive manner to foreign antigens
–immune system responds to self antigens
1-3=antibody mediated
4=T cell mediated.

102
Q

Hypersensitivity type 1-describe. 2 main cells involved? When antigen is first extractive, activates what? Then T helper cells stimulate B cells. These produce abnormally high levels of what. WHAT IS THIS CALLED? IgE binds to what?

A 
true allergy. When exposed to allergen, immediate physiological response within minutes-allergic response. 
IgE and mast cells. 
Ag spec T cells. 
IgE antibodies=ATROPY OR ATOPIC
mast cells.
103
Q

Mas cells can be in ? and ?.
What does IgE do that degrans mast cells.
Immediate release of? Hours later (late phase?)

A

mucosal or CT.
crosslink
histamine, serotonin, tryptase, leukotrienses, protease, etc.
Cytokines.

104
Q

Allergic response depends on 2.
If reaction last months/years=is called?
Are allergies from genetics or env: what is the hygiene hypothesis.
What are some non specific and immunotherapies?

A

dosage and route.
chronic response.
less hygiene=protection against develpment of atopy.
non spec-anti IgE, anti IL 5, anti hist, corticosteroids.
immunother-switch from Th2 to Th1=IgE to IgG. Diff antigen form. Diff route/conc.

105
Q

Define type 2 hypersensitivity. Most common Ex.
Explain transfusion with this.
Drug allergies
hemolytic anemia of newborsn.

A

when IgG (IgM) Abs attach foreign Ag associated with cells and cause destruction by phag or lysis. Often on RBCs. 1-2 hr reaction time.

bind to non-self bblood group antigens.
some drugs like antibiotics bind to the surface of RBCs and anti drug Abs cause RBC destruction
RBC Ag of the fetus stim Ab prod from mothers.

106
Q

What happens in direct and indirect Coombs.

A

Direct-take blood, add non human Abs. If anti human Abs bind to cell Abs= agglutinations.

Collect donor serume and add to cells of donor. Patients Ab bind donor RBCs. Add anti human Abs and RBcs agglutinate.

107
Q

Type 3 hypersensitivity define-

Complex can deposit somewhere like a BV and cause what. (neutrophils can degran by them too.

A

IgG Abs attack foreign antigens in a soluble form-results in immune complexes and EXTENSIVE inflamm/complement. 1-2 hr reaction time.

vasculitis, nephritis, and athritis.

108
Q

What are the 4 type 3 clinical exs covered.

A

Serum sickness-admin of anti venom serum from immnized horses.
drug induced-response to certain antibiotics.
Infection dz and
arthus reaction (skin test)

109
Q

Type 4 hypersens. Describe. How long does it take?

A

T cells directly recognize foreign antigens and cause inflamm and tissue injury. Takes up to 24 hrs (delayed) after 1-3 due to antigen specific T cells.

110
Q

In type 4, what T cells involved, what antigen, what does T cell do?

A

TH1-cell associated antigen. Activated macrophages against allergic contact, dermatitis, Tb.
CTL-cell associated antigens Cytotox. Graft reaction, allergies, poison ivy, etc.

111
Q

What is a contact hypersensitivity. What is a delayed type hypersensitivity

A

contact-highly reactive chemical that come in contact with skin and can modify self proteins resulting in a CD4 adn CD8 response.

Delayed.skin testing assays performed as a diagnostic test for mycobacterium infection.

112
Q

Define autoinflamm dz.

Define autoimmunity.

A

–unregulated inflammation resultting from an idiopathic dz, or a dz with unknown cause. Ex chrohns, inflamm bowel dz

Failure of the immune system to differentiate the body’s own cells and proteins from foreign substances, triggering inflamm response against self. Breakdown in central and peripheral tolerance.

113
Q

Specific causes of autoimmunity can be split into two categories. Give some ex for inf/environ.
What is molecular mimicry?
How does gender/hormones play a role?
Sequestered antigens?

A

Genetic factors and infection/environmental exposure.
Infection, diet, chemicals, drugs
–similarities between self and foreign antigens.
–more dzs happen in females.
–these antigens are normally not seen by the immune system, so T and B cells not deleted or inact during tolerance induction. Tissue damage/inflamm ensues. (immunopriv sites-eyes, brains, testis).

114
Q

What are the two ways autoimmune dzs are classified?

A

By primary immune components involved (2-4 hypersensitivies) primarily all Ab causes (2-3) but type 1 diabetes is T cell induced.
And by localized(organ specific) vs systemic

115
Q

Type 2 antibody against cell surface Ag: Autoimmune hemolytic anemia is a reaction against what antigens? Describe warm vs cold.

A

Blood group Ag.
Warm: more common. IgG and extravasc hemolysis via macrophages.
Cold: IgM and complement cascade causes intravasc hemolysis. Common in appendages during cold weather.

116
Q

Type 2 autoimmunity contd. Explain acute rheumatic fever
Myasthenia gravis?
Graves dz?

A

Ab against streptococcal cell wall, but (molecular mimicry) Ab attacks heart tissue causing rheumatic fever.

  • -Antagonistic antibody against Ach receptors-block Ach-impaired muscle contraction
  • -Agonistic–enhances TSH receptor fxn. Chronic release of thyroid hormone.
117
Q

Type 3 autoimmune-complex diseases-explain systemic lupus-

Type 4 autoimmunites-T cell mediated-explain Type 1 diabetes

A

immune complexes settle all over body and cause reaction.

T cell reacts with pancreatic Beta cell surface antigen and kills it. Decreased insulin prod.

118
Q

Canine allerigic dermatitis: 4 covered?

Define atopic dermatitis. Pathogenisis is complex and not well understood but involved 2 dysfunctions.

A

Atopic dermatitis, food allergic dermatitis, flea bite allergy, contact allergy
Hereditary chronic inflamm and allergic pruritic skin disorder.
immunologic and skin barrier

119
Q

Immunological dysfxn: What type of hypersens in atopic demititis. explain
predom of Th1 or Th2? Effect? What bears the IgE?

A

Type 1. IgE Ab against env allergens.

Th2–> IL 4 and 5. 4 causes B cell IgE secretion. 5 causes activation of eosinophils. Langerhans cells bears these IgE

120
Q

What are the 2 deficiencies involved in atopic dermatitis skin barrier dysfxn?
How is AD sensitized? Mode

Define food allergy dematitis.

A

ceramid and fillagrin def.
Resp and trans epi.

chronic pruritic inflamm and allergic skin disorder. One or more allergens in food.

121
Q

Pathogenesis of food allergy not well understood. Which types of hypersens?
Hx of AD and food are pruritis, skin lesions, what ages? When does each occur. So therefore, what is the issue?

A

1, 3 4
6 mnths-3 years
AD-year round or seasonal Food-year round

LOOK EXACTLY ALIKE

122
Q

As AD and food allergy Dz continue, what infections occur?

How to diagnose AD and food alllergy?

A

2ndary
AD-rule out food allergy, sarcoptic mange, flea bit allergy (allergy panel)
Food-food elim trail 8-10 weeks, food challenge 2 weeks. No skin or serum tests

123
Q

What are the Txs (3) for AD and food?

A

identify and treat 2ndary infection
for AD get specific immunotherapy, for food-novel or hydrolyzed diet
–give antipruritic or immunotherapy for both-glucocorticoids, anti histamines, EFAs and cyclosporins

124
Q

Flea allergy dematitis is what types hypersens? what is the allergen? What helps in diagnosis? How do you tx?

A

Types 1 and 4.
Flea saliva
intradermal test, presence of flea or flea dirt, response to flea control

tx: treat all animals, house and yard. Glucocorticoids

125
Q

What type of hypersens is contact dermatitis.

2 ways to diagnose?

A

Type 4

Avoidance of trigger or patch test.

Host Defense (2 decks)

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