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Immunology > Immuno CCOM 3 > Flashcards

Immuno CCOM 3 Flashcards

1
Q

What do Leukotrience C and D do?

A

smooth muscle contraction
increased vasc. permeability
mucus secretion
Leukotriene B formation

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2
Q

What does Leukotriene B do?

A

chemotactic for neutrophils

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3
Q

Oxidation of arachidonic acid via cyclooxygenase yields what?

A

PGs

thromboxanes

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4
Q

Oxidation of arachidonic acid via lipoxygenases yields what?

A

Leukotrienes C and D

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5
Q

What do PGs and thromboxanes do?

A

vascular and smooth muscle tone
platelet aggregation
immune reactivity

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6
Q

What does Platelet Activating Factor do?

A

platelet aggregation and secretion
neutrophil aggregation
degranulation
O radical release

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7
Q

What does TNF-a do in allergy repsonses?

A

actiavtes endothelium extravasation

proinflammatory

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8
Q

What are the 3 events characteristic of asthma?

A
  1. reversible obstruction (mucous)
  2. brochial hyperresponsiveness
  3. inflammation
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9
Q

What are the 3 possible lethal outcomes of Type 1 hypersensitivity and why?

A
  1. asphyxiation - largyngeal edema
  2. suffocation - bronchiole constriction
  3. shock - overwhelming peripheral edema
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10
Q

How do antihastamines work?

A

compete with histamine for H1 and H2 receptor sites on effector cells
Used prophylactically

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11
Q

What does chromalyn sodium do?

A

stabilizes mast cell membranes and prevents degranulation prior to exposure of allergen

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12
Q

What do corticosteroids do?

A

Prevents arachadonic acid pathways –> prevents late phase reactants

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13
Q

Which cytokines stimulate eosinophil growth and differeentiation?

A

GM-CSF
IL-3
IL-5

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14
Q

How does Omalizumab work?

A

humanized anti-IgE Ab

Inhibits binding of IgE to FceRI on mast cells and basophils

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15
Q

How does Singulair work?

A

Leukotriene receptor antagonist

Blocks action of Leukotriene D4 on CysLT1 receptor

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16
Q

What is the timing of initial and late phase repsonses in T1H?

A

initial: minutes

late phase: hours

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17
Q

Describe the hyposensitization technique

A

injection of diluted allergen with increasing concentrations over months

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18
Q

What are the theorized mechanisms for hyposensitization?

A
  • blokcing Abs are formed (IgG) and will bind up and remove allergens before they reach IgE
  • CD8 T-suppressor cells induced
  • Switch from Th2 to Th1
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19
Q

Describe desensitization (ie to antibiotics) and how does it work

A
  • Administer allergen increasingly over hours
  • Trigger sublethal doses of histamine release from mast cells, to deplete them of granules so larger therapeutic dose can be given
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20
Q

What are some classic examples of T2H?

A

Transfusion reactions
Rh incompatibility
drug induced reactions
some autoimmunes

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21
Q

Briefly describe T2H

A

Involved INSOLUBLE antigens( cells or tissue) and Abs of IgM or IgG.

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22
Q

What mechanisms are involved in T2H?

A
  • classical complement and lysis
  • opsonic effects of Fc and C3b receptors
  • occasionally ADCC
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23
Q

What does the term ‘secretors’ mean?

A

A and B antigens are present in mucopolysaccharides in secreionts like salive and sweat
- about 80% of people

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24
Q

Describe the dominance of the blood group alleles

A

A and B are dominant over O

A and B are codiminant to each other

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25
Q

How are isohemaglutanins believed to arise?

A

from colonization of gut in first couple years. They induce cross-reacting Abs against ABO blood antigens
-Evidenced by babies lacking anti-A or anti-B when theyre young

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26
Q

What type of Ig class are isohemaglutinins?

A

IgM

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27
Q

Briefly describe ADCC

A

Directly lysis of host cell via killer cells

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28
Q

On what other cells are Rh andtigens expressed?

A

none

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29
Q

What are the presentations of hemolytic disease in the newborn?

A 
anemia
leukopenia and thrombocytopenia
hepatomegaly
splenomegaly
ascites and edema
petechia
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30
Q

What is the mechanism of RhoGam?

A

It binds to and removes fetal RBCs from the mother’s immune system prior to initiating a response against Rh

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31
Q

What is a potential treatment if Rh sensitization occurs with a fetus?

A

intrauterine transfusion or exchange transfusion with O- blood

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32
Q

What can happen from a major injcompatibility in a blood transfusion?

A

If complement is activated, rapid lysis can occur causing anaphylaxis (not IgE mediated). Shock and death can happen

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33
Q

Briefly describe T3H

A

Allergic reactions involving deposition of immune complexes with activation complement. SOLUBLE antigens.

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34
Q

What is the Arthus recation>

A

localized deposition of insoluble IC
High IgG levels
subcu or intradermally or IM
Reaction 1-2 hours after injection

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35
Q

What are the cilnical manfestations of the Arthus reaction?

A

Gross: local swelling, hemorrhage or necrosis at center of lesion from vessel blockage
Acute Inflammatory repsonse: neutrophils, thrombi w platelets,

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36
Q

What is the mechanism of local response in an Arthus reaction?

A

Ag-Ab complexes get too big
Fc regions bind Ig and activate complement
C5a and C3a increase permeability
C5a chemoattractant.
Neutrophils frustrated phagocytosis
Release protesases, collagenase, O- intermediates…

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37
Q

Briefly describ sserum sickness syndrom

A

a systemic reaction to Ag give intravenously

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38
Q

What is the time of onset for serum sickness?

A

sensitized: hours to 4 days (anamnestic)

non-sensitized: 7-14 days (primary)

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39
Q

What is the relative Serum CH50 level during serum sickness? Why?

A

Reaches its lowest level because complement is being fixed and consumed quicker than it can be produced

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40
Q

When do T4H reaction soccur?

A

24-48 hours in a sensitized person

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41
Q

What is the key manifestation/distinction in T4H?

A

indurations - cutaneous or subcutaneous hardening

they do not ‘give’

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42
Q

What is an allograft and will there be rejection?

A

Donor and recipient are histoincompatible or nonhistocompatible
Graft rejection is expected

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43
Q

Why do you not need tissue typing for corneal transplants?

A

Cornea has immune privilege

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44
Q

What do you give before a peripheral blood transplant?

A

pretreatment with colony stimulating factors (CSFs)

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45
Q

What are the steps for am allogenic bone marrow transplant?

A

CSFs enrich donor HSCs
anti-mitotic drugs
irradiation (alblation)

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46
Q

What are first set rejection and second set rejection?

A

graft from histoincompatible (allograft or xenograft) leads to rejection after two weeks. Second graft from that donor rejected in one week

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47
Q

What would you witness for an athymic individual receiving a transp;lant>

A

No rejection of allografts or xenografts

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48
Q

When does a hyperacute rejection occur? What is it caused by?

A

Within a few hours
Preformed Abs to incompatible MHC or blood groups
NO cell mediated immunity

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49
Q

What is the mechanism of hyperacute rejection?

A

Binding of Abs induce complement cascade –> platelets–> thrombosis–> hemorrhage–> necrosis. Loss of function. Remove organ

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50
Q

When does acute rejection occur? What is it caused by>

A

within a few days. complete within 14 days.

Caused by T cell mediated immunity from mismatch of HLAs. Also maybe Abs against graft

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51
Q

When does chronic rejectino occur? What is it caused by?

A

months to years
initial activation of CD4
Then macrophages, CD8, Abs, classical complement, ADCC…

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52
Q

During which type of allograft rejection will exhibit lymphoid proliferation and follicles?

A

Chronic rejection

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53
Q

How would immunosuppresive thearpy work in chronic transplant rejection?

A

It would be useless

the damage has already taken place

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54
Q

What is Graft vs Host disease

A

donor lymphocytes attacking recipients tissues

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55
Q

What is the Graft-versus leukemia effect?

A

Some donor HSC preparations and T cells recognize minor histocompatibility or tumor specific antigens. These donor cells attack and kill leukemia cells

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56
Q

On which cells are HLA-1 expressed?

A

all nucleated cells

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57
Q

On which cells are HLA-2 expressed?

A

some HSCs (DCs)
thymocytes
Inducible in others via IFN-gamma

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58
Q

How many alleles of HLA does a normal human have?

A

12

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59
Q

What is the type of dominance in HLA genetics?

A

co-dominantly expressed (one haplotype inherited from each parent)

60
Q

What is serotyping?

A

using Abs to determine differences bw HLA molecules

61
Q

What is the key initiating event in acute allograft rejection?

A

The Recipient’s CD4 cells recognize the donor’s nonself HLA-2 on grafted tissue
(Passenger leukocytes from donor can also express HLA-2)

62
Q

What is direct recognition?

A

Mere recognition of nonself HLA even without processed foreing peptide on HLA

63
Q

What is indirect recognition?

A

The recipients APCs process donor antigens and present the to T cells

64
Q

What are the most potent transplantation antigens?

A

HLA-2 molecules

particularly HLA-DR

65
Q

With which type of HLA molecule would you see the longest graph survival?

A

HLA-DR

66
Q

What are the main mechanisms involved with graft rejection/HLA expression?

A

1) CD4 activation
2) recipient CD8 activation (IL-2)
3) Type 1 response (cytokines TH1)

67
Q

What does IFN-gamma do in transplantation?

A

Activation of macrophages

HLA-2 expression

68
Q

What does TNF-B do in transplantation?

A

cytotoxic to graft cells

69
Q

Which cytokines increase HLA-1 expression and result in cytolysis of transplanted cells?

A

IFN-gamma
IFN-alpha/beta
TNF-a
TNF-B

70
Q

Which organ transplants are particularly dependent on HLA matching

A

Kidney and bone marrow allografts

71
Q

When might you see graft rejection even if the donor adn recipient are an HLA match?

A

differences in minor histocompatibility antigens

72
Q

Where are the polymorphic regions on HLA genes?

A

Class 2: Exon 2

Class 1: Exons 2 and 3

73
Q

What do corticosteroids do?

A 
Inhibit gene expression
down regulate adhesion receptors
inhibit phagocytosis
inhibit HLA expression
Often given with antimetabolites
74
Q

What do Antimetabolites do?

A

Inhibit lymphocyte proliferation
purine antagonists
DNA alkylating agents
methotraxate

75
Q

What are some examples of antimetabolites?

A

azathioprine-purine antagonist

cyclophosphamide- DNA alkylating agent

76
Q

What are some blockin agents for immunosuppression?

A

monoclonal Abs against CD3 and against IL-2R (CD25)

77
Q

What does cyclosporine do?

A

Interferes with gene transcription in T cells - inhibits cytokine production
More effective when given before transplant

78
Q

Which drugs are similar to cyclosporine?

A

FK 506 (Tacrolimus) and rapamicin

79
Q

Which is the most critical antigen to match in transplantation?

A

the ABO blood group

80
Q

What happens if a person previously exposed to a tumor is introduced to a new tumor of the same type?

A

Anamnestic response

81
Q

Which cell is particularly important for tumor cell surveilance?

A

NK cell

82
Q

What is the immune seurveillance theory?

A

Mechanisms resopnseible for allograft rejection have evolved primarily as a means to defend against spontaneously arising neoplams

83
Q

In what situations are Abs good at attacking tumors? When are they not?

A

good: single cell tumors or metastases
bad: large or encapulated fibrous ones where Abs cant access

84
Q

Which Ig classes can lyse tumor cells?

A

IgG and IgM

85
Q

When can tumor cells be phagocytosed?

A

When they are opsonized by IgG

86
Q

Which Ig is usually used in ADCC? How does ADCC work?

A

Ig
K cell uses its Fc receptor to bind IgG
Apoptosis ensues

87
Q

What is the most important end line defense against tumors?

A

CD8 - HLA1 mediated killing

88
Q

What are lymphokine activated natural killer cells?

A

mostly NK cells from blood of cancer patients.
Grown in IL-2 and then transfused back
Allows immune system to escalate in vitro before in vivo

89
Q

What are Tumor Infiltratin Lymphocytes?

A

NK cells and some T cells from tumors.

Cultured in IL-2 and tranfused back with more IL-2

90
Q

What is the role of CD4 cytoines in tumors?

A

activate macrophages
induce CD8 activity
upregulate HLA-1 on tumor cells
upregulate HLA-2 on APCs

91
Q

What does IFN-gamma do in tumor?

A

attracts and activates macrophages
prevents emigration of macrophages
Upregulates HLA-1 and HLA-2

92
Q

What does immunologically privileged mean? Ex?

A

Cells of the immune system do not have access to certain compartments
ex: eye, brain, gonads, outer skin

93
Q

How do activated macrophages destroy tumor cells?

A

TNF-a

lysosomal enzymes

94
Q

How do tumor cells employ active immune suppression?

A

Production of soluble factors:
PGs
IL-10
TGF-B

95
Q

What are some of the effects of TGF-B when tumors secrete it?

A

inhibits Th1 response
decrease NK cell activity
inhbit antigen uptake
dampens CD4 and CD8 function

96
Q

Describe the antigenicity of a tumor cell that survives surveillance?

A

Usually the least antigenic because it can avoid the immune system

97
Q

What are blocking factors used by tumor cells?

A
  • Coat themselves in polysaccharides
  • Secreted Ags bind up Ab in circulation
  • Blocking Abs coat tumor cells to avoid CD8 recognition/killing
98
Q

What is Rituximab?

A

Anti-CD20 to target B cells in B cell lymphomas

99
Q

What is Her2/neu?

A

targets tumor cells in breast and ovarian cancers

100
Q

What is Cetruximab?

A

anti-EGFR against colorectal and head/neck cancers

101
Q

What is Zevalin?

A

murine Ab that targets CD20 on small tumors

Releases MoAb toxin

102
Q

What is trastuzumab/Herceptin?

A

-anti-ErbB-2 that attaches to cancer cell and targets it
-also tells that cancer cell to stop growing and proliferating
Depletes target cells w opsonization, complement, ADCC
receptor blockers

103
Q

What is Tositumomab? What is used to treat?

A

anti-CD20 conjugated to Iodine 131

Treats non-Hodgkin lymphoma

104
Q

Which cells are involved in tolerance?

A

B and T cells

105
Q

What are the two mechanisms for Central B cell tolerance?

A

Clonal anergy for soluble antigens

Clonal deletion for insoluble

106
Q

Describe peripheral B cell tolerance

A

Escaped B cells receive constant low level stimulation of the BCR in absence of any other secondary signals –> anergic
-Also they are barred from lymphoid follicle in nodes, so ithey dont get survival signals

107
Q

What type of peptides are the ones presented on MHC in the thymus?

A

Self-peptides

108
Q

Where does central T cell toelrance occur?

A

thymus

109
Q

Primary stimulation of T cells without secondary stimulation leads to what?

A

functional inactivation - clonal anergy

They can never be activated even if they encounter antigen

110
Q

What happens when CD28 and B7 dont associate

A

Since CD28-B7 signal stabilizes IL-2 mRNA, there is a lack of IL-2 production –> anergy

111
Q

Repeated stimulation of activated T cells reults in what?

A

Can cause T cell to undergo apoptosis - clonal deltion

112
Q

Is B or T cell tolerance quicker?

A

T cell toelrance is quicker

113
Q

What are the main mechanisms of Peripheral T cell tolerance?

A

lack of CD28-B7 signal
Fas-FasL expressed
pro-apoptotic proteins

114
Q

How can you distinguis Tregs?

A

They express FoxP3, a transcription repressor

115
Q

What are the mechanisms of Treg cells?

A

Inhibitory cytokines:
Th1-Th2 couterregulation
TGF-B: anitinflammatory that suppresses T cell proliferation
Cell lysis also used

116
Q

How do Breg cells work?

A

The produce IL-10 that negatively regulate the activation of Th1 CD4 cells and CD8 cells. This dampens autoreactivity

117
Q

Which diseases demonstrate low levels of IL-10?

A

Multiple slerosis

SLE

118
Q

Describe immune responsiveness with regards to age?

A

the very young and old are immunosuppressed

AI diseases occur commonly after puberty

119
Q

What is one of the main causes of Ai diseases?

A

malnutrition

120
Q

How does stress influence the immune resonse?

A

heat schock proteins are upregulated by stressed cells
Increased Ag presentation
gamma/delta T cells recognize this

121
Q

What dosage levels of an antigen induce toelrance?

A

very high or very low doses over long periods of time

122
Q

What is sympathetic ophthalmia?

A

When a perforated ocular injury allows access of immune molecules to immune privileged site and autoimmune response generated

123
Q

What is Ag sequesteration?

A

self molecules are hidden from the immune system in immunoprivileged sites

124
Q

What anatomical locations demonstrate Ag sequesteration?

A

lens of eye
synovial chondrocytes
spermatozoal antigens

125
Q

How does immunogenicity relate to tolerance?

A

Weak immunogens (less complex and soluble) readily induce tolerance

126
Q

What are some examples of molecular mimicry?

A

Strp pharyngitis-rheumatic fever
Camp. jejuni - Guillan barre
Klebsiella - AS

127
Q

What are the histological changes in Celiac Disease?

A

villus atrophy
T cell infiltration
(T cell mediated)

128
Q

What is Celiac Disease associated with?

A

Abs against tissue transglutaminase
HLA-DQ2 (or HLA-DQ8)
IgA deficiency

129
Q

How does gender influence autoimmunity?

A

Women are more likely

Estrogen receptors on immune cells may play a role

130
Q

Describe Myasthenia Gravis

A

Abs produced against ACh receptors at neuromuscular junctions. Severe muscle weakness. HLA-DR3

131
Q

What is lazy leukocyte syndrome?

A

Defefct in neutrophil response to chemotactic factors or a deficiency in production of C3a and C5a

132
Q

What is the defect in Chronic Granulomatous Disease?

A

X linked recessive
cytochrome b and NADPH oxidase defects
(G6PD and myeloperoxidase defect can also cause this)

133
Q

What is the defect in Chediak Higashi Syndrome.

A

mutation in LYST generesulting in defect in lysozome generation and function. Neutrophils and CTL are defective.

134
Q

What is Bruton’s X linked agammaglobulinemia?

A

recurrent infection from bacteria that produce antiphagocytic capsules
normal pre B cell level but low mature B cell level
Defect in BTK gene (BCR signaling)

135
Q

What is X linked hyper-IgM syndrome?

A

high IgM levels. Rest are low
CD40L mutation
autoAbs for neutro, RBCs
pyogenic infections

136
Q

What are the general physiologic effects of anaphylaxis?

A

periphery: vasodilation and smooth mm relaxation

bronchoconstriction in lungs and GI

137
Q

Which cell types play a significant role in asthma?

A

gamma/delta TCR

eosinophils

138
Q

What are the three main groups that T1H mechanisms are grouped in?

A

Sensitization
Activation
Effector

139
Q

Which organs stimulate a stronger IgE response when presented with an allergen?

A

respiratory
GI
skin

140
Q

Which age groups are predisposed to immediate hpyersensitvity and asthma? Why?

A

very young and very old (rare)

probably related to thymus development - peaks in size at puberty

141
Q

What are some common polymorphisms for allergies?

A

IL-13
IL-4R
CD14
HLA

142
Q

What is the difference bw FceRI and FceRII?

A

FceRI: high affinity - mast cells/ basophils
FceRII: low affinity- platelets, lymphs, mono, eosins

143
Q

How does the mast cell slow down degranulation during T1H?

A

influx of Ca increases cAMP and cGMP. This signaling slows down degranulation

144
Q

What are the clinical manifestations of histamine release?

A

increased vasc perm.
edema
pruritis
increased exocrine secretions

145
Q

What are the preformed mediators that are released from a mast cell?

A

Histamine
Eosinophil activating factor
Proteases/Hydrolases
Heparin

146
Q

What are the newly synthesized mediators that are released from a mast cell?

A 
Arachidonic acid
Leukotrienes B, C, D
PGs, thromboxanes
Platelet Activating Factor
IL4, IL13, TNFa, GM-CSF

Immunology (7 decks)

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