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Host defense > Jim Hays final exam review > Flashcards

Jim Hays final exam review Flashcards

1
Q

What is type I hypersensitivity?

A

Allergic reaction

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2
Q

What is type II hypersensitivity?

A

Specific monoclonal antibodies produced against host tissue antigen. Examples of Type II: Good Pasture’s, Antibodies against platelets or RBCs

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3
Q

What is type III hypersensitivity?

A

An excess of antigen leads to immune complex accumulation that is not effectively cleared from the circulation leading to deposition. Examples of Type III: Lupus, Arthus reaction, serum sick syndrome

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4
Q

What is Type IV Hypersensitivity?

A

Delayed hypersensitivity, TMMI

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5
Q

Describe what is happening in an Arthus reaction

A

LOCAL reaction- Antibody accumulation due to previous infection/vaccination results in massive IC formation upon subsequent exposure to antigen, overwhelming RBC transport, causing massive neutrophil activation by IL-8 and complement components

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6
Q

IC recruits this leukocyte to site of infection

A

Neutrophil

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7
Q

What two inflammatory pathways does IC activate?

A

FcR-gamma crosslinking on macrophages and complement activation

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8
Q

Describe etiology of systemic immune complex disease, and what are its net effects on the body

A

IC binding to vascular C3b and Fc receptors, recruiting PMN via IL-8, activating inflammatory complement components

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9
Q

ITAM

A

Immunoreceptor tyrosine-based activation motif. FcgR present on phagocytes. very high affinity for IC. Induces phagoytosis

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10
Q

ITIM

A

FcgR on B cells. low affinity for IC. Inhibits B cells activation at high levels of Ag-Ab

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11
Q

Where are MCt mast cells predominantly found?

A

Mucosa

MCt = Mast cell tryptase

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12
Q

Where are MCtc mast cells predominantly found?

A

Epithelium (CT)
MCtc = tryptase and mast cell-specific
chymase

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13
Q

IgE class switching cytokines?

A 
IL4 and IL13
Promotion of IgE class switching occurs by up regulation of CD-23 (FcεRII receptor) on mast cells and basophils that increase their production of IL-4 and IL-13. This is strongly influenced by gene influenced polymorphisms.
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14
Q

Name cytokine responsible for IgA class switching

A

TGF-beta, (IL5)

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15
Q

What is the cytokine profile in allergic reactions?

A

IL4, IL5, IL13

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16
Q

What is the onset of the early phase of Type I hypersensitivity after antigen exposure, and what is necessary for it to occur at all?

A

Occurs within 15 min antigen exposure. Dependent on previous exposure and sensitization. Inflammation due to complement activation and leukotriene/prostaglandin release

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17
Q

What is the onset of the late phase of Type I hypersensitivity after antigen exposure, and what does the reaction depend on?

A

Occurs within hours of antigen exposure. Dependent on Th2 activation and the presence of cytokines IL3, 4, 5, 13, TNF-_, GM-CSF and IL-10. Eosinophils present now.

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18
Q

List important eosinophil chemotactants

A

eotaxin, IL5 augments effect

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19
Q

Most important factor for allergy diagnosis

A

Careful history taking

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20
Q

What is the RAST assay?

A

Radioallergosorbent test- ELISA for serum IgE binding to solid allergen

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21
Q

List 3 ways superantigens differ from conventional antigens

A
  1. They can react with MHC class II in unprocessed form
  2. React with side of MHC class II and BCR/TCR
  3. Induce an immediate primary polyclonal response in T cells
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22
Q

What cells make up synapse I of the germinal center reaction, and where does it occur?

A

Naive CD4 T cell: Mature DC

Deep cortex of lymph node

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23
Q

What cells compose synapse II in the germinal center reaction, and where does the synapsing occur?

A

Antigen-primed B cell: Antigen-specific CD4 T cell

Near edge of follicle in lymph node

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24
Q

What cells will you find in synapse III of the germinal center reaction?

A

High affinity centrocyte: TFh (Follicular helper CD4 T cells)

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25
Q

List two CCR7 (commonly found on T cell) ligands

A

CCL19 and CCL21

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26
Q

What upregulates LFA-1 on lymphocytes in the HEPCV and what does LFA-1 bind to?

A

CCL21 upregulates LFA-1 on lymphocytes

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27
Q

Name a naive T cell receptor that binds endothelium and the naive T cell CD profile

A

L-selectin (binds CD34, promotes lymph node localization)

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28
Q

Name two effector T cell receptors that bind endothelium and the effector T cell CD profile

A

LFA-1 (binds ICAM-1) and VLA-4 (binds VCAM-1)

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29
Q

Why do DC’s migrate to lymph nodes after antigen TLR activation?

A

upregulation of CCR7, follow CCL19 and CCL21 gradient

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30
Q

Cytokine necessary for centrocyte differentiation, Class switching & Antibody secretion during the germinal center reaction

A

IL-21

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31
Q

IgG class switching cytokine?

A

IFN-gamma

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32
Q

List four IgA functions

A
  1. Barrier to pathogen invasion of mucosa
  2. Intracellular pathogen neutralization
  3. Excretion of invader from lamina propia into GI lumen
  4. Provides passive immunity to infant GI tract through breast milk
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33
Q

IgA deficiency: describe symptoms and associated diseases. Is IgA therapy a good idea in these patients?

A

Sx: often asymptomatic, but could present with FMH of IgA deficiency, high incidence of oral infection, frequent respiratory infection, chronic diarrhea

Assoc.: Lupus, rheumatoid arthritis, thyroiditis
Avoid IgA therapy! Host will produce anti-IgA antibodies

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34
Q

List two C3 convertases

A

C4b2a- Classical and Lectin pathway

C3bBb- Alternative pathway

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35
Q

Infection associated with MAC defect

A

Neisseria sp only

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36
Q

What history of illness may be seen in a patient with a defect in the Lectin complement activation pathway?

A

recurrent childhood bacterial infections

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37
Q

List two C5 convertases

A

C4b2a3b- Classical and Lectin pathways

C3bBbC3b- Alternative pathway

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38
Q

What does CD59 normally inhibit in the complement system, and what is the result of a CD59 defect?

A

Normal function is to prevent MAC formation

Defect results in RBC lysis- paroxysmal nocturnal hemologinurea

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39
Q

Describe the normal function of C1INH in the complement system, and the result of a C1INH defect.

A

Normal function is to inhibit C1 activity by decoupling C1q from C1r and s.
Deficit results in Hereditary Angioneurotic Edema- fluid accumulation, epiglottal swelling, abdominal attack

40
Q

What is the consequence of a defect in the classical complement activation pathway?

A

IC disease

41
Q

What is the consequence of a defect in the alternative complement activation pathway?

A

Infection with Neisseria spp and pyogenic bacteria

42
Q

List one C3 convertase inhibitor (there are others, but he really only emphasized one)

A

DAF- delay accelerating factor

43
Q

Name some C5 convertase inhibitors

A

Factor I, Factor H, CR1

44
Q

What type of infections will you see in someone with a defect in C3b deposition?

A

Infection with pyogenic bacteria and Neisseria spp

45
Q

Name 2 functions of C5a.

A

Leukocyte chemotaxis

Degranulation of Mast and Basophils along with C3a and C4a - anaphylatoxins, increases vascular permeability

46
Q

Describe the mixed lymphocyte culture lab technique used in transplant immunology.

A

Mixing the serum of 2 patient’s together in a medium containing radioactive thymidine. One patient’s serum is inactivated so that their lymphocytes will not be able to proliferate. Any radioactive uptake by cells will be the result of responder lymphocytes from one host proliferating in response to the MHC of stimulator APC’s from the other host.

47
Q

Why is the “direct” alloimmune response by the host to a transplanted organ a heresy?

A

Violates the dogma of MHC restriction. Donor APC’s migrate to secondary lymphoid tissue and activate naive CD4 T cells using their MHC II alone as the antigen- no antigen processing, and not recognized in the context of the HOST’S MHC

48
Q

Hyperacute transplant rejection- time frame, why is the reaction so strong and fast?

A

Occurs within 48 hours of transplant.
Swift rejection due to presence of recipient alloantibody from previous exposure. Source of previous reaction against MHC could be multiple pregnancies, blood transfusions. Incorrect blood type matching can also precipitate rejection (type O getting a Type A or B organ- will have antibodies against A and B already)
Severe graft ischemia results from complement and coagulation mediated endothelial destruction, as well as leukocyte infiltration.

49
Q

Acute onset transplant rejection- time frame and mechanism of rejection

A

Appearance of donor-specific immune effector cells within 3 weeks of transplant.
DTH- Type IV TMMI reaction. CD4 Th1 cells mediate the TMMI and activate CD8’s but TH17 and B cells are also involved.

50
Q

Characteristic vascular changes seen in chronic rejection

A

Hallmark of chronic rejection is diffuse, widespread arteriolar narrowing caused by intimal thickening of the vessel- mechanism unknown

51
Q

What epitope presents a barrier to xenotransplantation?

A

Alpha-GT. We lost this gene when we stopped being monkeys, have antibodies against it, all other animals have it

52
Q

What HLA type does trophoblastic tissue display, and what does it do?

A

HLA-G, has an inhibitory motif for maternal NK’s

53
Q

What’s different about maternal NK cells in the gravid uterus?

A

Stimulated by TGFb and progesterone to become inhibitory to other immune cells- produce anti-inflammatory cytokines, lack Fc receptor for ADCC (CD16)

54
Q

Why is mom susceptible to viral infections during pregnancy?

A

High levels of circulating progesterone and IL-10 suppresses Th1 responses. Lack of TMMI, also Th17 and cytotoxic response

55
Q

Name 3 proteins important in bone remodeling

A

RANK, RANKL, OPG

56
Q

What immune responses are pro-clastogenic?

A

Th1 and Th17

57
Q

Name the 4 adipocytokines

A

Leptin, adipoleptin, MIC-1, visfatin

58
Q

List the anti-inflammatory adipocytokines

A

MIC-1 (macrophage inhibitory cytokine-1) and adiponectin

59
Q

List the pro-inflammatory adipocytokines

A

Leptin and visfatin

60
Q

Pro-inflammatory cytokine and strong m/m chemotactant

A

osteopontin

61
Q

M2: pro or anti inflammatory?

A

Anti

62
Q

M1: pro or anti inflammatory?

A

Pro

63
Q

Net state of inflammation in non-obese WAT?

A

Slightly anti-inflammatory

64
Q

What type of macrophages dominate WAT in obese people, and what is the net effect on health?

A

M1’s rule! Stuffing of adipocytes promotes pro-inflammatory signaling and recruitment of macrophages via osteopontin/CCL2, which recruit more.

65
Q

Why is a fatty artery an example of local obesity?

A

Cholesterol in plaques recruit M1 macrophages, which recruit more M1’s via CCL2/osteopontin and prevent them from leaving

66
Q

What type of cells mediate brain host defense, and why is inflammation bad in the brain?

A

Microglial cells- type M2, held in active suppression by TGF-B and IL10.

Activation by PAMPs (infection) or DAMPS (head injury) leads to M1 conversion, inflammatory response damages surrounding neurons.

67
Q

What 3 highly polymorphic molecules determine the variations in the immune response between individuals?

A

MHC’s, TLR’s, cytokines (and their receptors)

68
Q

What do you need to know about an infection before you make a vaccine for it?

A

What type of infection it is- do you need to promote a Th1, Th17, Th2?

69
Q

Name 3 ways that tumor cells can “look different” immune effector cells

A

Mutation of self proteins displayed in their MHC
Over expression of self-protein in MHC
Modification of self-proteins in MHC

70
Q

How do tumor cells evade destruction or detection?

A

Secrete CC21, recruit and convert to T cells to Tregs, which become trapped in the tumor tissue, setting up a immunosuppressive shield around it. LIKE A GIANT DEATH STAR OF IMPERIAL IMMUNOSUPPRESSION

Tumors upregulate PD-L1/2 on cell surface- induces death to all T cells with PD-1 receptor

71
Q

Tumor cells have T regs protecting them. What is the only part of the immune system that is still capable of attacking the tumor?

A

“Save us NK Cell, you’re our only hope!”

Will only work if the tumor cell forgot to close its exhaust vent- the MHC-I displaying tumor specific antigen. Otherwise it should be just like shooting womp rats back home.

72
Q

In response to stress, what neurotransmitters effect the release of CRH from the hypothalamus?

A

Epi, NE, GABA, Ach, SE

73
Q

What lymphoid tissues are directly stimulated by the nervous system (as opposed to indirectly by the neuroendocrine system)?

A

Bone marrow- NE

74
Q

Effect of cortisol on the immune system?

A

anti-inflammatory: reduced cytokine production, T and B cell reactivity, NK cell activity

75
Q

Effect of epi and NE on the immune system?

A

Increase leukocyte mobilization to peripheral blood
Thymus- NE, Ach, peptidergic
Spleen- NE
Lymph- NE, peptidergic

76
Q

Effect of beta endorphins and enkephalins on the immune system?

A

Increase T and NK cell reactivity

77
Q

What triggers the acute mobilization/recruitment of lymphocytes to the blood in response to stress?

A

Epi, NE

78
Q

What triggers the redistribution of lymphocytes to the lymph nodes 1-2 hours after exposure to stress?

A

Epi/NE in combination with cortisol

79
Q

Effect of acute stress on DTH response?

A

Enhances it

80
Q

Effect of chronic stress on DTH response?

A

Depresses it

81
Q

Effect of low dose cortisol on DTH response?

A

Enhances it by increasing lymphocyte redistribution to the lymph nodes

82
Q

Effect of high dose cortisol on DTH response?

A

Depresses it by suppressing immune function

83
Q

In what direct and indirect ways (list 2) can the immune response affect the CNS?

A

Direct: IL-1, IL-6, TNF interaction with neurons after passing through the BBB
Indirect: stimulation of vagal afferents by IL-1

84
Q

How does the nervous system attenuate the immune system to prevent excessive inflammation?

A

Splenic nerve: NE–> T lymphocyte in spleen: Ach–> macrophages inhibited from releasing inflammatory cytokines

85
Q

What effector mechanisms of the immune system are involved in both bacterial and viral infections?

A

PMN, macrophages, Ab+complement opsonization, Ab+complement lysis, antibodies blocking absorption of pathogen into tissue

86
Q

What effector mechanisms are specific to bacterial infection?

A

Neutralization of toxins by antibody

87
Q

What effector mechanisms are specific to viral infection?

A

CTL and NK cytolysis of infected cells, IFN alpha and beta anti-viral protection

88
Q

What 2 proteins do IFN alpha and beta upregulate?

A

Synthetase and protein kinase

89
Q

A wild Candida albicans appeared! Name the type of pathogen and the immune response the body will choose.

A

Extracellular fungi. I choose you, cytokine activated phagocytes!

90
Q

A wild Influenza virus appeared! Name the type of pathogen and the immune response the body will choose.

A

Obligate intracellular virus. I choose you, everything!

91
Q

A wild Streptococcus pneumoniae appeared! Name the type of pathogen and the immune response the body will choose.

A

Extracellular bacteria. I choose you, antibodies, complement and phagocytes!

92
Q

A wild Neisseria meningitidis appeared! Name the type of pathogen and the immune response the body will choose.

A

Extracellular bacteria. I choose you, antibodies, complement and phagocytes!

93
Q

The toxin of a wild Clostridium tetani appeared! Name the type of pathogen and the immune response the body will choose.

A

Tetanus toxin. I choose you, antibody! Antibody used neutralization…. critical hit!

94
Q

A wild Mycobacterium tuberculosis appeared! Name the type of pathogen and the immune response the body will choose.

A

Intracellular bacteria. I choose you, Th1 cells and activated macrophages!

95
Q

A wild Schistosoma mansoni appeared! Name the type of pathogen and the immune response the body will choose.

A

Extracellular parasite. I choose you, antibody, complement and eosinophils! Eosinophil used ADCC…one hit KO!

Host defense (9 decks)

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