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Host Defense > Test 2, deck 2 > Flashcards

Test 2, deck 2 Flashcards

1
Q

what is an exaggerated or misdirected immune response called, and what are the 4 types

A 
"hypersensitivity disease" 
type 1: allergies/asthma (IgE) 
type 2: diseases caused by antibodies directed against tissue antigens (hemolytic anemia) 
type 3: immune complex diseases (lupus) 
type 4: TMMI problems
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2
Q

what is an immune complex? what is its role?

A

binding of an antibody to its antigen; role= facilitation & amplification of both humoral and cellular defenses to pathogens

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3
Q

what does the formation of an IC depend on?

A
  • intensity of antigen stimulus, including:
    1) type of antigen
    2) length of host exposure
    3) route/site of exposure
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4
Q

what influences the rate of IC formation?

A
  • rate of antibody formation
  • antibody avidity (how well it sticks)
  • valence of antigen
  • complement & Fc/FcR interactions
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5
Q

what does the vigor of an immune response depend on?

A
  • gender (women= huge response to B cell antigens)
  • age
  • MHC
  • immune related genetic loci
  • polymorphisms of Fc receptor genes
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6
Q

most important inflammatory reaction

A

binding of (antigen+IgG) to FcgammaR on monocytes and neutrophils; aggregation of ICs on surface of bacteria allows for cross-linking of receptors

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7
Q

what two inflammatory amplifying systems can an IC activate?

A

1) FcR crosslinking

2) complement (classic or direct)

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8
Q

how is IC mediated inflammation controlled?

A
  • antigen exposure is reduced (antibiotics)
  • catabolization of Ics by neutrophils/macs after binding FC receptor
  • free IC bound RBC and transported to liver
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9
Q

describe the erythrocyte transport of ICs

A
  • IC-C3b form complexes
  • C3b can bind to the CR1 (on all peripheral blood cells except platelets)
  • C3b converted to iC3b (inactive)
  • goes to liver and is removed by fixed macrophages (kupffer cells) OR
  • goes to spleen to activate B cells
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10
Q

what happens if formation of IC> destruction?

A

“Free” IC will activate multiple inflammatory amplifying systems locally & systemically
(especially Fc activation and complement)

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11
Q

what happens to circulating ICs not on RBCs?

A
  • activates local neuts and macs in endothelium (commonly kidney/skin/synovium)
  • releases Il8 which recruit more neuts to area & activates complement pathway
  • destroys vasculature & tissues
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12
Q

how is IC mediated inflammation controlled?

A
  • antigen exposure is reduced (antibiotics, drainage)
  • catabolization of Ics by neutrophils/macs after binding FC receptor
  • free IC bound RBC and transported to liver
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13
Q

what is an Arthus reaction?

A
  • occurs when there are high levels of pre-existing antibodies to the antigen introduced under the skin (e.g. repeated immunization)
  • get rapid accumulation of immune complexes, lots of neutrophil activation
  • get pain, swelling, redness at site of antigen infection
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14
Q

what is acute serum sickness?

A
  • give foreign serum to treat rattle snack venom
  • body starts making antibody against serum
  • formation of serum proteins + anti-serum antibodies exceeds disposal
  • get fever, vasculitis, nephritis, arthritis (depending on site of IC deposition) and reduced complement levels (high IC formation)
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15
Q

what is the problem diagnosing IC disease? what can be used?

A
  • wide variation in complexes
  • typically diagnosed clinically
  • newer assays try to look for activated C3
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16
Q

3 treatments for IC disease

A
  • eliminate antigen (drain, take antibiotics)
  • inhibit antibody formation
  • suppress inflammation
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17
Q

what happens when IC goes to the spleen (via RBC receptors) or lymph nodes (via lymph)

A
  • not efficient site for disposal

- extremely potent stimuli for antibody production

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18
Q

describe immunoregulation by Fcgamma receptors on APCs

A
  • only recognize antibody with something in FAB
  • cross-linking by antibodies activates ITAM
  • cell is prompted to phagocytose the complex
  • receptor affinity is high, can be activated by small amount of IC
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19
Q

describe immunoregulation by Fcgamma receptors on b-cells

A
  • receptor affinity is low, needs lots of IC
  • complexes cross link Fcgamma receptors and activate ITIM
  • ITIM is a negative signal, shuts down further B-cell proliferation
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20
Q

how is the Rh problem prevented?

A

give mother IgG antibody to bind with fetal red cells, turns off B-cells that are anti-fetal RBC by tricking them into thinking they’ve made enough, CD4 and B memory cells are not generated

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21
Q

describe the Rh problem

A
  • 1st pregnancy: Rh- mother exposed to Rh+ antigen from baby, forms anti-Rh antibodies, has primary response
  • 2nd pregnancy: maternal IgG (including anti-Rh) crosses placenta and destroys fetal red cells, has secondary, more intense response
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22
Q

what happens if you get Rh- mom IgM anti-Rh?

A

won’t work, because you want to be targeting the Fcgamma response; IgM will stimulate more IgG

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23
Q

an allergic response is a type ___hypersensitivity reaction

A

type 1

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24
Q

define atopy

A

the ability to transfer reactivity to allergens by means of

serum; genetic predisposition to develop IgE antibodies upon exposure to environmental allergens

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25
Q

what cells express high affinity for IgE FcE receptors constitutively? what are they full of?

A
  • mast cells and basophils

- vasoactive mediators like histamine and leukotrienes

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26
Q

how are mast cells categorized and where are they found?

A

2 major subtypes:

  • tryptase (MCT cells) - mucosa of respiratory & GI tracts
  • tryptase and mast cell-specific chymase (MCTC cells)- connective tissues (dermis/submucosa) of GI tract, heart, conjunctivae, perivascular tissues
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27
Q

how is IgE induced? common component of environmental antigens?

A
  • by environmental proteins (“allergens”) found in insects, worms, shellfish and foods and fungi that can induce hypersensitivity responses in atopic individuals
  • MHCII D genes, in concert with other non-MHC genes, promote IgE production over IgG responses by influencing the type of TLR activated, type of T-helper cell and cytokine milieu present during allergen presentation by APC
  • chitin ( a polysaccharide not found in mammals)
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28
Q

how do genetics influence allergies?

A
  • 50% of individuals with two allergic parents will also be allergic
  • multiple genes act together to produce an allergic response
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29
Q

describe the context of antigen exposure required to develop an allergy?

A
  • high level of exposure early in life coupled to a lack of exposure to other infectious disease antigens
  • route- delivery of antigens in small amounts to mucosal surfaces
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30
Q

sequence of an allergic response

A
  1. contact allergen (usually mucosal)
  2. uptake of allergen by DC w/ “allergic” TLR; get production of IL-4
  3. allergen presented in MHC Class II
  4. Th-2 activation occurs
  5. IL-4 is dominant cytokine, allergen-specific B-cells activated (lots of IL4 & 13)
  6. Promotion of IgE class switch by upregulating Cd-23
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31
Q

T/F FC on IgE can bind FCRs on mast cells and basophils without antigen

A

TRUE- STRONG (20,000 x stronger than IgG binding its FC receptor)

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32
Q

what is the immediate phase of the type 1 hypersensitivity reaction?

A
  • occurs within 15 minutes of allergen exposure (MUST be exposed before)
  • allergen binds IgEs already on mast cells/basophils
  • vasoactive mediators are released
  • prostaglandins and leukotrienes are synthesized/released
  • complement activation by tryptase released from mast cells
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33
Q

what is the late phase of the type 1 hypersensitivity reaction?

A
  • occurs within hours of allergen contact
  • completely dependent on Th2 activation
  • characterized by infiltration of the site by eosinophils, neutrophils, mast cells, basophils, lymphocytes
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34
Q

what cytokine increases FcER display, augmenting the IgE reaction?

A

Il-5

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35
Q

describe the hygiene hypothesis?

A

early exposure to childhood
illnesses “sets” normal Th1 and Th2 responses to subsequent environmental antigen exposure; lack of early exposure is associated with lack of Tregs

36
Q

What is the most important factor for arriving at a correct allergy diagnosis?

A

a careful clinical history

37
Q

what happens to your cardiovascular system with anaphylaxis?

A

heart rate spike, blood pressure drops- die b/c of hypotension

38
Q

describe the RAST assay

A
  • patients serum added to cellulose disc with bound antigen
  • IgE present in serum binds to antigen
  • wash, add radio labeled anti-IgE, radioactivity counted with a gamma counte
39
Q

autograft, isograft, allograft, xenograft

A
  • self-to-self, accepted
  • identical twin to twin, accepted
  • person to person, variable degrees of rejection (“allogenic graft”)
  • species to species, strong rejection
40
Q

3 types of donors

A

living-related
living- nonrelated
cadaver

41
Q

describe the complement-dependent cytotoxicity assay and what its used to tests

A
  • tests for recipient’s antibodies to donor
  • take patients serum and incubate with a panel of lymphocytes of known HLA specificity
  • if there are antibodies, they will bind to MHC antigen on lymphocyte cell surface
  • add complement, which lyses known pairs (bad
42
Q

describe the mixed lymphocyte culture

A
  • assess recipients T-cell proliferation against donor
  • mix recipient’s lymphocytes with irradiated donor lymphocytes (only role is to display MHC)
  • cells incubated for 5 days, add radioactive precursor of DNA
  • if recipient’s t-cells don’t proliferate, get no radioactive uptake= no interactions = OK for donation
43
Q

what does the intensity of rejection depend on?

A

1) differences in MHC (especially class 2)
2) the host’s immune response genes
3) physician intervention (drugs)

44
Q

what is the difference between direct and indirect alloregulation?

A

direct- recipient’s APC takes up antigen, presents it in MHCII, presents to T cell

indirect- donor’s APC migrate to lymph node, recipient’s T cells recognizes MHCII as antigen

45
Q

what’s a passenger leukocyte?

A

leukocytes present in donor tissue (E.G. dendritic cell) migrate to spleen, activate T cells, which migrate to graft and kill it

46
Q

what can be the trigger for specific rejection?

A

1) antigen picked up by host B cells
2) donor dendritic cells presenting self-peptide which looks like antigen
3) antigen picked up by host dendritic cells

47
Q

what happens after specific rejection has been triggered?

A

1) activated macrophage mediated graft destruction
2) CD8 specific graft cytolysis
3) Th17 mediated inflammation ** if dominant, will be more destructive (more neuts)
4) antibody mediated graft destruction

48
Q

what are some reasons hyperacute rejection occurs?

A
  • (often) occurs immediately after graft placement, recipient has alloantibody before transplantation (mis-match in blood type)
  • can be sensitized by multiple pregnancies, blood transfusions
49
Q

what happens with hyperacute rejection?

A
  • get rapid binding of antibodies to antigens on transplant epithelium, platelets aggregate at site of damage
  • platelets secrete mediators for coagulation cascade, graft becomes ischemic
  • neutrophils attracted to ischemia , cause clotting
  • complement escalates whole clotting situation
  • graft turns pale
50
Q

what happens with acute rejection?

A
  • immune cells appear in graft during the first 3 weeks after grafting
  • CD4 t-cells react with antigens and mediate TMMI response
  • antigen-specific T cells attack graft
  • Th17 promotes inflammation
  • B cell antibody appears `
51
Q

what is the hallmark of chronic rejection?

A

repeated episodes of rejection; diffuse, widespread arteriolar narrowing, fibrosis; eventually leading to graft ischemia

52
Q

how do gene arrays help with rejection diagnosis?

A

take biopsy of organ, distinguishes between acute & chronic rejection & drug toxicity

53
Q

when does graft-vs-host disease occur?

A
  • when bone marrow is transplanted and the T cells attack recipient’s tissue
  • or when immunoincompetent host recieves a transfusion
  • to test, use reversed mixed lymphocyte culture
54
Q

what gene prevents xenotransplantation?

A

alpha-1,3-galactosyl; get hyperacute rejection

55
Q

what does fetal tissue at the materal-fetal interface down regulate? what does it up-regulate, and what does that do?

A

down-regulates normal MHC complexes (I and II)

up regulates MHC-G, inhibits cytotoxicity of NK cells

56
Q

what do placental NK cells produce?

A
  • are special NK cells*
  • TGF-B and IL-10 (for regulatory effects)
  • angiogenic factors
57
Q

what do you find in high concentrations in uterine wall?

A
  • special NK cells
  • gamma delts
  • paternal antigen-specific T-regs
58
Q

what happens to maternal lymphocytes that access fetus?

A

converted to T regs

59
Q

what is the clinical implication for mother during pregnancy

A
  • progesterone + placental derived factors suppress local & systemic Th-1 responses
  • lack of Th1 predisposes mom to viruses (e.g. flu, TB)
  • if converted to Th1 bias, can lose fetus
60
Q

what happens when the fetus is infected?

A

high presence of Tregs can lead to tolerance to the infecting pathogen, can prevent child from responding appropriately later

61
Q

what are 4 key benefits of commensal microbiota?

A
  1. required for development of the immune system (germ-free animals have almost no secondary lymphoid tissue)
  2. provide energy by metabolizing polysaccharides
  3. provide vitamins
  4. protect from pathogens
62
Q

what balance does a healthy intestinal microbiota generate?

A

Th1/Th17 : Tregs

63
Q

what does dysbiosis of the gut contribute to?

A

inflammatory bowel disease, autoimmunity, allergy, obesity

64
Q

what can dysbiosis be caused by?

A

diet, antibiotics, stress, early childhood exposure, genetics

65
Q

what should not be given with cancer drugs?

A

antibiotics -killing commensals decreases chemotherapy effectiveness

66
Q

what can IBD be treated with?

A
  • is T-cell mediated inflammatory response
  • treat in mice by giving B. fragilis, inducing an anti-inflammatory response (by inducing Tregs); shows promise with mouse MS as well
67
Q

what is the hygiene hypothesis?

A
  • increase in allergy due to decreased exposure to microbes during childhood
  • Th1 responses down-regulate Th2 (IgE producing) responses
68
Q

what happens if you co house mice with obesity associated microbiota and lean associated microbiota and feed them a low fat diet?

A

They both get lean!

69
Q

T/F Cecarean delivery results in vaginal microbiota

A

FALSE- skin microbiota

70
Q

3 ways superantigens differ

A

1) can react with MHCII in unprocessed form
2) activate outside the peptide binding groove- is on the side, like a TCR-MHC bridge
3) elicit an immediate primary polyclonal response in T-cells

71
Q

what do superantigens cause?

A
  • massive outpouring of pro-inflammatory cytokines

- can lead to cytokine storm syndromes & systemic toxicity

72
Q

what cytokines do you see a lot of with a superantigen response?

A

INF-gamma & TNF alpha

73
Q

viruses required a living host for propagation; 3 ways they evade destruction?

A
  1. down regulate TLRs
  2. produce inhibitory signals for NK cells
  3. produce soluble cytokine effectors to bind up cytokines before they act
74
Q

factors that play role in autoimmunity

A

gender (females 85%), genes, environment

75
Q

what percentage of siblings with diabetes share 2 HLA haplotypes? 1? 0? what is the normal ratio?

A

60: 35:5
25: 50:25

76
Q

if a TCR reacts with an AIRE protein what happens?

A
  • it is converted to a protective CD4, CD25 Treg
77
Q

what is Treg function controlled by? what is it reliant on?

A

CTLA-4 (acts as brake); reliant on IL-2 from exogenous sources

78
Q

things that could lead to an autoimmune disease

A
  • inadequate display of AIRE
  • loss of CTLA4 gene
  • loss of FoxP3 function
79
Q

non-T cell source of autoimmunity

A
  • TLR over-expressed/under-expressed/mutated

- DC function impaired

80
Q

how could a viral infection initiate an autoimmune disease?

A
  • infect cells (e.g. beta cells) and initiate CD8 attack against them
  • display antigens that look like Beta cells so the CD8s attack
  • incite collateral damage
81
Q

if something is chronic with lots of neutrophils, which immune effector cell do you suspect?

A

Th17

82
Q

what are the initiation cytokines for Th17

A

TGFbeta, IL23, Il6 (last 2 prevent T regs)

83
Q

what inhibits the development of Th17s?

A

INFgamma, IL4

84
Q

what does IL17 do?

A

recruits neutrophils

85
Q

what normally happens to self-reactive B cells?

A
  • checking is less stringent, normally die from neglect because no t-cell can activate them
86
Q

T/F All autoantibodies cause disease

A

FALSE- if find autoantibodies in blood of women, not necessarily lupus

Host Defense (6 decks)

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