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micro exam 3 > Tumor Immunology Hypersensitivity > Flashcards

Tumor Immunology Hypersensitivity Flashcards

1
Q

What is a tumor

A

An abnormal growth resulting from uncontrolled proliferation with no physiologic funtion

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2
Q

other name for a tumor

A

Neoplasm (new growth)

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3
Q

What is Cancer

A

Malginant tumor

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4
Q

Difference between Benign and Malignant Tumors

A

Slow growth: Rapid Growth
Well-defined capsul: Not encapsulated
Not invasive: invasive
Well differentiated: pooly differentiated (anaplasia)
Low Mitotic index: High Mitotic index
Does not metastasize: Can spread distantly (metastasis)

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5
Q

what is cancer a predominantly a disease of

A

Aging

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6
Q

How does Cancer proliferate

A

Clonal

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7
Q

why does cancer spread so rapidly

A

as a mutation it is benifical to the cell to grow fast, so it has a selective advantage ocer its neighbored (increased groth or decreased apoptosis)

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8
Q

What needs to occur to have Full blown cancer

A

4-7 mutations in a step wise accumulation of alterations occuring in specific genes

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9
Q

What are Carcinogens

A

Agents that can cause genetic mutation or alterations of gene expression that can lead to the development of cancer

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10
Q

Examples of Carcinogens

A

Chemical (Alcohol, asbestos, benezene, tobacco, aluminum)
Radioactive (plutonium-239, radon-222, iodine-131)
Pathogens (Epstein-Barr Virus, H. pylori, Hep B and C, HPV)

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11
Q

What do Cancer-Causing Mutations affect

A

Activation of growth-promotion pathways
Block antigrowth signals
Prevent apoptosis
Turn on telomerase and new blood vessel growth
Allow tissue invasion and distant metastasis

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12
Q

What are tumor associated antigens

A

Normal proteins that are expressed in abnormally high levels, in an abnromal location, or during an abnormal stage of cellular development

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13
Q

What are tumor specific Antigens

A

Macromolecuels (PR or carbs) that are unique to the tumor

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14
Q

What suppresses many developing malignancies

A

An efficient immune system

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15
Q

Defects in the immune system increase the risk of what type of cnacer

A

Viral assocaited

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16
Q

What is antitumor immunity

A

Innate and adaptive responses that can contribute to tumor destrucution and elimiation

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17
Q

Can Tumors evade the immune system

A

Yes

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18
Q

What is Protumor immunity

A

Evidence that some immune responses can perpetuate tumor development (Chronic inflammation)

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19
Q

Innate cells invovled in Antitumor Immunity

A

MAcrophages (M1)
Neutrophils (N1)
Dendritic Cells
NK cells

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20
Q

What can innate antitumor cells recognize

A

DAMPS that may be upregulated during tumor growth

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21
Q

How do DAMPS forom tumors contribute to inflammation

A

Via IFN gamma, IL-12, TNF-alpha, ROIs, and RNIs

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22
Q

How are NK cells activated to a tumor

A

IFN gamma

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23
Q

What are Nateral Killer Cells biolgoically

A

Lymphoid cells that contain perforin and grnzymes

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24
Q

what do NK cells recognize

A

MHC I but are not ag specific

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25
Q

What is the ROll of NK cells in fighting off tumors

A

Important for removing virally-infected and tumor

cells

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26
Q

How to NK cells kill

A

Antibody binds antigen on the surface of target cells
Fc Receptors on NK cell recognizes bound antibody
Cross linking of Fc Receptors signals the NK cells to kill the target
Target cell dies by apoptosis

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27
Q

What drives the Th1 response to tumors

A

IFNgamma and IL-12

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28
Q

what lymphocytes are invovle in adaptive antitumor immunity

A

Cytotoxic T lymphocytes (CTLs)

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29
Q

What must be broken for a T cell to be invovled in ANtitumor immunity

A

A break in central tolerance in order for a T cell to be involved

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30
Q

Cells in Protumor Immunity

A 
MAcrophages (M2)
Dendritic CElls
Regulatory T cells
Th2 cells
Myeloid-derived suppressors cells
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31
Q

Roll of Macrophages (M2) in protmor Immunity

A

PRomote Angiogenesis and invasiveness

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32
Q

Roll or Dendritic cells in Protumor Immunity

A

Suppress T cell functions

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33
Q

Problem with inflammation relation with cancer

A

an important factor in the development of cancer

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34
Q

what does Active inflammation do for cancer

A

Predisposes a person to cancer by stimulating a wound-healing reponse that includes proliferation and new blood vessel growth

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35
Q

Susceptible organs to get cancer from inflammation

A

GI tract, Pancrease
Thyroid gland
PRostate, urinary bladder
Pleura, skin

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36
Q

Anti-tumorigenic effect of Dendritic cell

A

Release Cytotoxic Cytokines

Antigen presentation to T cells

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37
Q

PRo-tumorigenic roll of Dendtriic Cells

A

Suppress T cell function

Promote tumor growth and progression

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38
Q

Anti-Tumorigeneic role of T cells

A

Directly lyse cancer cells

Release cytotoxic cytokines

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39
Q

Pro-tumorigenic roll of T cells

A

Release tumor promoting cytokines

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40
Q

Anti-tumorigenic Roll of Treg

A

Restor homeostasis to reduce chronic inflammaion

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41
Q

Pro-tumorigenic roll of Treg

A

Suppresses anticancer immune responses

Stimulate inflammatory cytokine producion

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42
Q

Anti-tumorigenic roll of macrophages

A

RElease cytotociv cytokines

Antigen presentation to T cells

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43
Q

PRo-tumorigenic roll of MAcrophages

A

PRomote Angiogeneisis, tumor proliferation, chemotaxis, invasiveness, and metastis

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44
Q

Anti-tumorigenic roll of Myeloid derviced suppressor cells (MDSC)

A

Limited

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45
Q

Pro-tumorigenic Roll of MDSC

A

Suppress T cell function

REcruit immunosuppressive immune cells

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46
Q

Anti-tumorigenic roll of NK cells

A

Relase Cytotociv cytokines

Directly Cytotocix to Cancer cells

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47
Q

Pro-tumorigenic roll of NK cells

A

Limited

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48
Q

Conventional Cancer treatmetns

A

Surgery
Chemo
Radiation

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49
Q

When is surgery not good for cancer treatment

A

NOt good for diffuse cancers

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50
Q

Problem with Chemo to treat cancer

A

Non-specific

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51
Q

How does Chemo fight cancer

A

TArgets rapidly growing cels, but can also damages normal cels too such as immune cells, GI and Hair

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52
Q

Benifit of Ratiation over Chemo

A

More target than Chemo

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53
Q

How does Radiation Work to fight cancer

A

Radioactive substances generate ROIs that can severely damage tumor DNA causign the cells to die

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54
Q

Why is Monoclonal Ab good to fight cancer

A

Advantageous due to specificity, but first need to find a specific target

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55
Q

what must be found to use Monoclonal Ab

A

Tumor specific or tumor-associated antigens

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56
Q

What is HErceptin (trastubzumab) used to treat

A

Breast cancer treatment for patients with tuomrs that overexpres HER2

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57
Q

What is HErceptin (trastuzumab)

A

A monoclonal Ab that binds to HER

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58
Q

How does Herceptin work

A

PRomotes NK cell mediated ADCC

INterferes with HER2-directed Signa that promote tumor growth

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59
Q

How to do adoptive T cell transfer therapy

A

Remove T cells from patient
–Isolate T cells taht recognize cancer or T cell can be genetrically engineered to recognize cancer cells
Clonally expand cancer-specific T cells
Infuse PAtient with Cancer specific T cells

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60
Q

Types of Adoptive T cell transfer therapies

A

TIL (Tumor Infiltrating Lymphocytes)
TCR (T cell receptor)
CAR (Chimeric Antigen Receptor)

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61
Q

What type of Adoptive T cell transfer is the most advances

A

CAR T cell therapy

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62
Q

What is the main side effect of CAR T-cell therapy

A

Cytokine relase syndrome in which a patient feels flu symptoms for 5-7 days

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63
Q

What is CAR T-cell therapy approved for

A

PEdiatric Acute lymphoblastic Leukemia (ALL) and for adult with advanced lymphoma

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64
Q

3 main causes of hypersensitivies

A

Reaction to Sself (autoimmunity)
Reaction against Micrboes
Reaction against Envirnomental Antigens

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65
Q

Other name for Type persensitivityI HY

A

Allergy, Atopy, immediate hypersensitivity

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66
Q

when does Type I hypersensitivity occur

A

within minute after reexposure to antigen/allergen

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67
Q

What is The Type I Hypersensitivity response

A

Rapid IgE and Mast cell mediated vascular and smooth muscle reaction that is often followed by inflammation

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68
Q

What determines what reactions may affect due to type I hypersensitivity

A

depending on the route of allergen entry

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69
Q

Commonness of Tyep I hypersensitivity

A

Most common disorder of the immune system of about 20% of the population

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70
Q

Typr I hypersesnsitivity General sequence of envents

A
  1. Initial exposure to antigen and production of IgE antibodies
  2. Binding of IgE ab to Fc receptors on mast cells
  3. Cross-linking of bound IgE upon reexposure to allergen
  4. Release of mast cell mediators
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71
Q

What is Sensitization

A

Intial exposute to antigen and production of IgE antibodies in Type I Hypersensitivty

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72
Q

What occuring in Sensitization

A 
Antigen presention to Th2 cell or Tfh cell
Antigen bound B cell and Il-4 and CD40L causes class switching to IgE
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73
Q

Release of Mediators from mast cells in Type I Hypersensitivity leads to what

A

A biphasic Response

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74
Q

What are the Immediate Effects of Type I hypersensitivity

A

Dilation of Bloodvessel, increased vascular permeability, and smooth muscle contraction (the immediate reaction)

75
Q

what is the Late response of Type I hyper sensitivity

A

Inflammation (late phase reaction)

76
Q

What must bind to create Type I hypersensitivity

A

ANtigen-specific IgE

77
Q

The Immeidate REsponse of MAst Cell Degranulation

A 
Vasoactive amines (Histamines and sesroton) and Proteases
Synthesis and secretion of lipid mediators (prostaglandins and leukotrienes)
78
Q

what happens in the Late Phase reaction for MASt cell Degranulation

A

Synthesis and secretion of Cytokines (TNFalpha, IL-4, Il-5, GM-CSF) and Chemokines (MIP-1alpha)
Infiltration of eosinophils, monocytes, and nuetrophils

79
Q

What do Eosinophils that come in response to mast cell degranulation do

A

Release granules containing reactive oxygen species, prostaglandins and Leukotrienes

80
Q

Roll of Histamine and lipid mediates in Type I hypersensitivty

A

Vascular/smooth muscle response (immediate reactions)

81
Q

Roll of Cytokines in Type I hypersensitivty

A

Inflammation (late phase reaction)

82
Q

How common is Asthma

A

22 million americas, 6 millions

83
Q

how often does Asthma ,kill

A

80% of deaths occur in low to low mid income countries

84
Q

What does Asthma tend to do to someone

A

PRoduce extra mucus and breathing becomes hard

85
Q

What are the most common signs of ASthma

A

Coughing
Wheezing
Shortness of breath

86
Q

Triggers for Asthma

A

Airborne allergnes (pollen, animal dander, mold, corckroaches and dust mites)
Respiratory infections, such as common cold
Physical activity (exercise induced asthma)
Col air
Air pollutants and irritants such as smoke

87
Q

Why does Asthma make it hard to breath

A

Muscles of the broncial tunes tighten and thicken

Air passages become inflammed and mucus filled making the air difficult to move

88
Q

How is Asthma treated

A

Inhaled corticosteroids
Inhalaed long acting beta2 agonist
Leukotriene inhibitors
Cromolyn

89
Q

What is the most effective long-term control mediation for asthma

A

Inhaled Corticosteroids

90
Q

what is a inhaled corticosteroids

91
Q

How do Inhaled long actiing beta2 agonist fight asthma

A

Act on beta-adrenergic receptors to cause bronchodilation

92
Q

why use inhaled long-acting beta2 agonists

A

As a rescue medication

93
Q

What is an inhlaed long-acting beta2 agonist

94
Q

How do Leukotriene inhibitors work

A

Hlep block the chain reaction that increases inflammation in your airways

95
Q

example of Leukotreien inhibitors

96
Q

what is Cromolyn

A

Inhaled medication to help prevent mast cell degranulation

97
Q

what drives an anaphylaxis response

A

Driven by systemic release of vasoactive amines and lipid mediators from mast cells

98
Q

What does Anaphylaxis cause

A

Life-threatening drop in BP accompanied by severe bronchoconstriction

99
Q

how to treat anaphylaxis

A

Epinephrine (vasocontrictor and bronchodilators) and antihistamine

100
Q

THe most severe form of immeidate hypersensitivty

A

Anaphylaxis

101
Q

what leads to different immeidate hypersensitivty syndromes

A

Mediators produced in different amounts and in different tissues

102
Q

What is Type II hypersensitivty

A

Antibody Dependent Cytotoxicty

103
Q

what occures in Type II hypersensitivty

A

Antibodies produced by the immune response that bind to antigens on own cell srufaces

104
Q

What Antibodies tend to be involved in Type II Hypersensitivty

A

IgG and IgM isotypes

105
Q

Binding of IgG and IgM isotypes to their own Cell surface due to Type II Hypersensitivty results in what

A

Activate Complement result inmembrane attack complex formation, ultimately to destruction of cells, inflammation, or intereference with normal cellular functoin

106
Q

Target antigen of Autoimmune Hemolytic anemia

A

Erythrocyte membrane proteins

107
Q

Target antigen of Graves’ Disease

A

Thyroid-stimulating hormone (TSH) receptor

108
Q

Target antigen of Myasthenia gravis

A

Acetylcholine (ACH) receptor

109
Q

Autoimmune hemolytics anemia mechanism of disease

A

Opsonization and phagocytosis of erythrocytes, complement-mediated lysis

110
Q

GRaves’ disease mech of disease

A

Antibody-mediated stimuation of TSH receptors

111
Q

Myasthenia gravis mechanism of Disease

A

Antibody inhibits ACH binding to receptor leading to downregulation of receptors

112
Q

Clinicopathologic manifestations of autoimmune hemolytic anema

A

Hemolysis, anemia

113
Q

Clinicopatholgoic manifestations of Graves’ disease

A

Hyperthyroidism

114
Q

Myasthenia gravis Clinicopathologic manifestations

A

Muscle weakness

Paralyiss

115
Q

How does Hemolytic disease of the NEwborn work

A

1st baby has RBC’s with Rh antigen
mom has Rh-specific B cell that creates Anti-Gh IgM and Memory cells to fight it
2nd pregnancy not has IgG and antiRh ab crosses placenta and attacks fetal RBS’s leading to erythroblastosis fetalis

116
Q

Roll of Rhogam in fighting Hemolytic disease in the newborn

A

Prevents B cell activation and memory cell formation

117
Q

How to treat Autoimmaves Diseaseune hemolytic anemia

A

Corticosteroids or blood transfusion

118
Q

How to treat Hemolytic disease of the newborn

A

Rhogam injections (anti-Rh ab)

119
Q

How to treat Graves Disease

A

Radioactive Iodine, anti-thyroid drugs, or thyroid removal

120
Q

How to treat Myasthenia Gravis

A

Cholinesterase inhibitors and corticosteroids

121
Q

What is Type III hypersensitivty

A

Immune complex-Mediated

122
Q

a grouping of antigens bound to their specific antibodies

A

Immune complex

123
Q

where do Ag-Ab complex clump and deposit

A

In blood vessels or tissues attracting an acute inflammatory reaction

124
Q

what type of Immune complexes tend to be cleared by phagocytes

A

LArger immune complexes

125
Q

Where do small immune complexes tend to deposite

A

In blood vessels or tissues

126
Q

What do Small immune complexes act on

A

Ligate Fc receptors on leukocytes, leading to activation and tissue damage

127
Q

What kinds of Antigens can Cause Type III Hypersensitivity

A

Exogenous and endogenous antigens

128
Q

when does Type III hypersensitivty occur

A

within hours (3-10h) after exposure to antigen

129
Q

where do Type III hypersensitivity immune complexes tend to accumulate

A

at sites where antigen is localized

Sites of turbulence (vessel branches) or high pressure (kidney glomeruli and synovium)

130
Q

Because Type III Hypersensitivity locolize at sites of Turbulence and high pressure how does the disease manifest

A

Vaculitis, arthritis, or nephritis

131
Q

Diseases Caused by type III hypersensitivity

A

Systemic Lupus erythematosus
Post-streptococcal glomerulonephritis
Serum Sickness

132
Q

Antigen involved with Systemic Lupus Erythematosus

A

DNA
Nucleoproteins
others

133
Q

Antigens involved with Postr-streptococcal glomerulonephritis

A

Streptococcal cell wall antigens

134
Q

Antigens invovled with SErum sickness

A

Various proteins

135
Q

Clinical manifestation of Systemic lupus erythematosus

A

Nephritis, arthritis Vasculitis

136
Q

Clincial manifestation of Post-streptococcal glomerulonephritis

137
Q

Clinical manifestations of Serum sickness

A

Arthritis
Vasculitis
Nephritis

138
Q

Mechanisms of Type III Hypersensitivity

A

Mast cell activation
Macrophages release TNF_apha and IL-1 that induce the inflammatory cascade
Complement activation (C3a, C4a, and C5a)

139
Q

what does Complement activation of Type III Hypersensitivity do

A

Stimulate mast cels to release more histamine, serotonin, and chemotactic factors
Attracts monocytes, neutrophils, and other leukocytes

140
Q

Cells bearing Fc receptors for IgG (or IgM) and IgE may be crucial for what type of hypersensitivty

A

Antibody complex mediated hypersensitivity

141
Q

Causes of Serum SIckness

A

Antivenom (serum from horses immunized with snake venoms_
Anti-lymphocyte globulin
Antibiotics
Steptokinase (a bacterial enzyme)

142
Q

What is Antivenom

A

A source of Neutralizing antibodies to treat people with poisonous snake bites

143
Q

What is anti-lymphocyte globulin

A

Animmunosuppressive agent used for transplant recipients

144
Q

what is streptokinase used as

A

A thrombolytic agent used to treat heart attack patients

145
Q

How to treat serum sickness

A

Avoid drugs, antihistamines,corticosteroids

146
Q

Treating Lupus

A

NSAIDS, Corticosteroids, immunosuppressive agents

147
Q

What kind of Recation is Type IV hypersensitivity

A

Cell Mediated

148
Q

How does Type IV Hypersensitivity occure

A

Mediated by antigen-specific T cells which induce macrophage infiltration iin a sensitized individual

149
Q

What initiates Type IV Hypersensitivity

A

Haptens
Ag presented by APC’s activates Th cells
Th Cells secrete cytokines with activate macrophages

150
Q

what are haptens

A

Small molecules that must become bound to a larger carrier molecule in order to Illicit and immune or inflammatory responce

151
Q

How are Th Cells activated in Type IV Hypersensitivty

A

Ag presented by APC’s

152
Q

What is Type IV hypersensitivity also called

A

Delayed-type hypersensitivity (DTH) since the action takes 2-3 days to develop

153
Q

What antibodies mediated Type IV Hypersensitivity

A

Not antibodies (Mostly Th cells)

154
Q

what cells are important effector cells in the DTH response

A

Macrophages, CD8 T cells, and NK cells

155
Q

what do Activated CD8 cells do in Type IV hypersensitivity

A

Destroy target cells on contact

156
Q

How does CD* cells destroy target cells on contact

A

2 phases:
Sensitization
Elicitation

157
Q

when does Sensitiziation ocur

A

During the first exposure to Ag

158
Q

How long does Sensitization take to develop

A

Take 10-14 days

159
Q

what happens during Sensitization during Type IV hypersensitivity

A

Angitegn presenting cells take up AG and present to T cells

Formation of CD4+ memory T cells specific for the Ag

160
Q

When does Elicitation for type IV Hypersensitivity occurs

A

during reexposure to Ag

161
Q

when does Elicitation develop for type IV exposure

A

within 24-48 hour

162
Q

what happens in elicitation for type IV hypersensitivty

A

LC Ag presentaion to memory T cells at site of Ag entry
T cells release IGNgamma and Pro-inflammatory cytokines
Cytokines recruit macrophage, CTL, NK, and other efector cells

163
Q

Types of Type IV Hypersensitivity

A 
Tuburculin type hypersensitivity
Contact Dermatitis
Chronic Asthma
Gluten-sensitive Enteropathy
GRaft regjection
164
Q

How does one get Tuburculin type Hypersensitivity

A

Injected into the skin

165
Q

what mediates Tuburculin type Hypersensitivity

166
Q

How does one get Contact Dermatitis

A

Absorbed by the skin

167
Q

what mediates Contact Dermatitis

A

Th1 Cells and/or CTL’s

168
Q

How does one get Chronic Asthma

169
Q

what mediates Chronic Asthma

170
Q

how does one get Gluten-sensitive enteropathy

171
Q

What mediates Gluten-sensitive enteropathy

A

poorly understood but evidence suggest that Th1 and Th2 are involed

172
Q

what mediates Graft rejections

173
Q

HOw to test if previously exposed.infected with Mycobacterium tuberculosis

A

Tuberculin Test (Mantoux PPD test)

174
Q

how is the Tuberculin test done

A

Small amounts of Tuberculin are injected intradermally
24-72 hours a local T cell mediated inflammatory reactions evolves in individuals previously with Mycobacterium tuberculosis

175
Q

what mediates response in the Tuberculin Test

A

TH1 cells and infiltrating macrophages and other inflammatory mediators causing visible swelling and redness

176
Q

what type of hypersensitivity is Poison ivy

A

Contact dermatitis (type IV)

177
Q

what are the response parts of poison ivy

A

Sensitization period and elicitation of allergic response on subsequent interactions

178
Q

Common allergens associated with contact dermatitis

A 
Poison oak, poison sumac, plants
Nickel and other metals
MEdication (antibiotics especially topical, topical anesthetics plus more)
Rubber and latex
Cosmetics
Fabric and clothing
Detergents
SOlvents
Adhesives
Fragrances and perfumes
Other chem
179
Q

Therapeutic strategies for Type IV hypersensitivity for TB test injections

A

Usually self limiting

180
Q

trerapeutic strategy for contact hypersensitivity due to type IV

A

Limit exposure
Corticosteroids
Antihistamines

181
Q

Therapeutic stratogy for CHronic Asthma due to type IV hypersensitivity

A

Corticosteroids, bronchodilators, Cromolyn

182
Q

Therapeutic stratogy for Crohn’s disease

A

Corticosteroids
Immunosuppressants
Biologics

183
Q

How to remember what type of sensitivity is What

A 
I: Allergy
II: antiBody
III: immune complex
IV: Delayed (DTH)
ABCD

micro exam 3 (15 decks)

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