Infectious Disease - Immunology - Regulation; Hypersensitivity; Vaccines; Tumors Flashcards
(136 cards)
1
Q
CD___ is the main IL-2 receptor.
A
CD25 is the main IL-2 receptor.
2
Q
Treg cells have a ________ affinity for MHC II receptors presenting _____ antigens.
Upon binding these proteins, they do what?
A
Treg cells have a high affinity for MHC II receptors presenting ‘self’ antigens (endogenously synthesized proteins that have been picked up by APCs after leaking from dead cells).
Suppress the T cell response to reduce likelihood of autoimmunity (peripheral tolerance)
3
Q
True/False.
MHC II can sometimes present ‘self’ antigens.
A
True.
These are endogenously synthesized proteins that have been picked up by APCs after leaking from dead cells.
4
Q
__________ tolerance involves inactivation of overactive T cells in the thymus.
__________ tolerance involves TReg cells supressing immune activity in the periphery.
A
Central tolerance involves inactivation of overactive T cells in the thymus.
Periperal tolerance involves TReg cells supressing immune activity in the periphery.
5
Q
True/False.
Central tolerance in the thymus basically answers the question, ‘does the T cell bind MHC too tightly?’
A
True.
6
Q
Peripheral tolerance — TReg cells sense _______ cells and inhibit T cell activity.
A
Peripheral tolerance — TReg cells sense self cells and inhibit T cell activity.
7
Q
What is neonatal immune tolerance?
It is only relevant in what conditions?
A
The neonate becomes tolerant to anything it is exposed to at birth in non-inflammatory conditions
8
Q
Why is neonatal tolerance important?
A
The neonate is exposed to maternal antigens en masse during delivery and breastfeeding — it would be detrimental if the child developed immune activity against normal body proteins
9
Q
B7-CD28 interactions lead to IL-___ production.
A
B7-CD28 interactions lead to IL-2 production.
10
Q
What receptor, when expressed, decreases immune activity by binding B7 (on APCs) with a higher affinity than CD28?
What interleukin is especially down-regulated via this process?
A
CTLA-4;
IL-2
11
Q
Why do TReg often protect tumor cells from T cells and NK cells?
How do they accomplish this?
A
The tumor cells display ‘self’ antigens;
PD-1 receptor binding
12
Q
True/False.
PD-1 receptor activity promotes the killing of tumor cells by T cells and NK cells.
A
False.
PD-1 receptors (when activated by PD-L1) inhibit the killing of tumor cells.
13
Q
Anti-tumor immune activity can be increased by the administration of ___-__ inhibitors.
A
Anti-tumor immune activity can be increased by the administration of PD-1 inhibitors.
(PD-1 activity decreases the killing of tumor cells because they are self cells.)
14
Q
What cell type displays the Foxp3 transcription factor?
Defects in this surface receptor cause what condition?
A
TReg cells;
IPEX
(immunodysregulation polyendocrinopathy enteropathy X-linked syndrome)
15
Q
IPEX (immunodysregulation polyendocrinopathy enteropathy X-linked syndrome) is caused by a mutation in what TReg surface receptor?
How is this condition treated?
A
Foxp3;
immunosuppressive medications (lethal if not treatment not begun in early childhood)
16
Q
What rare X-linked disorder is characterized by pervasive autoimmunity affecting multiple organs?
A
IPEX
(immunodysregulation polyendocrinopathy enteropathy X-linked syndrome)
17
Q
B cells generally require ___ cells to enable them to mount autoimmune responses against self antigens.
A
B cells generally require TH cells to enable them to mount autoimmune responses against self antigens.
(I.e. virtually all autoimmunity is mediated by T cells.)
18
Q
What general cell type mediates virtually all autoimmunity?
A
T cells
(B cells generally require TH cells to enable them to mount autoimmune responses against self antigens.)
19
Q
Most autoimmune conditions are precipitated by some sort of _____________ event (e.g. stress, infection) that increases immune activity by increasing IL-_____ secretion.
A
Most autoimmune conditions are precipitated by some sort of inflammatory event (e.g. stress, infection) that increases immune activity by increasing IL-2 secretion.
20
Q
Autoimmunity is mostly mediated by what specific cell type?
A
TH1 cells
21
Q
What routes of antigen intake are typically tolergenic?
What routes are typically immunogenic?
A
Oral and IV routes;
subcutaneous, IM, intradermal
22
Q
What amount of antigen load (low, intermediate, high) is most likely to promote an immune response?
A
Intermediate
(1. Small amount of antigen –> tolerance (probably mimics normal dying of cells releasing small amounts of antigen at a time
2. High amounts of antigen –> tolerance (clonal exhaustion)
3. Intermediate amount of antigen –> immunogenicity)
23
Q
1. Small amount of antigen –> __________ (tolerance/immunogenicity).
2. Intermediate amount of antigen –> __________ (tolerance/immunogenicity).
3. High amounts of antigen –> __________ (tolerance/immunogenicity).
A
1. Small amount of antigen –> Tolerance (probably mimics normal dying of cells releasing small amounts of antigen at a time).
2. Intermediate amount of antigen –> Immunogenicity.
3. High amounts of antigen –> Tolerance (clonal exhaustion).
24
Q
Why do very small amounts of antigen often not lead to immune responses?
Why do very large amounts of antigen often not lead to immune responses?
A
Mimics normal dying of cells releasing small amounts of antigen at a time;
clonal exhaustion
25
\_\_\_\_\_\_\_\_\_\_ exposure to an antigen leads to clonal exhaustion leads to \_\_\_\_\_\_\_\_\_\_.
**_Persistent_** exposure to an antigen leads to clonal exhaustion leads to **_tolerance_**.
26
**True/False**.
Persistent exposure to an antigen can lead to tolerance.
**True**.
Due to clonal exhaustion.
27
\_\_\_\_\_\_\_\_ ________ --- an antigen-recognizing T cell accidentally activates a B cell that produces antibodies against a similar ‘self’ antigen.
**_Molecular_** **_mimicry_** --- an antigen-recognizing T cell accidentally activates a B cell that produces antibodies against a similar ‘self’ antigen.
28
**Molecular mimicry** --- an antigen-recognizing ___ cell accidentally activates a ___ cell that produces antibodies against a similar ‘self’ antigen.
**Molecular mimicry** --- an antigen-recognizing **_T_** cell accidentally activates a **_B_** cell that produces antibodies against a similar ‘self’ antigen.
29
All of the following are example causes of autoimmunity:
Molecular \_\_\_\_\_\_\_\_\_\_
Increased ______ antigens present on MHC II
\_\_\_\_\_\_\_\_\_proliferation / decreased \_\_\_\_\_\_\_\_\_\_\_\_\_
All of the following are example causes of autoimmunity:
Molecular **_mimicry_**
Increased '**_self_**' antigens present on MHC II
**_Lympho_**proliferation / decreased **_supression_**
30
Autoreactive antibodies bind cells, and then NK CD\_\_\_ are cross-linked as they bind the antibody ___ the cell is then killed.
Autoreactive antibodies bind cells, and then NK CD**16** are cross-linked as they bind the antibody **FC** the cell is then killed.
31
Delayed hypersensitivity:
1. Allergen is sensed in skin by a ________ cell.
2. The above cell travels to a **lymph node** where it activates a ________ cell.
3. This cell now enters the bloodstream and looks for signs of **inflammation**, at which point it enters the tissue.
4. The cell is now activated by a ________ and begins releasing cytokines.
5. **Eosinophils** follow the cytokines to the area.
Delayed hypersensitivity:
1. Allergen is sensed in skin by a **_dendritic_** cell.
2. The above cell travels to a **lymph node** where it activates a **_TH2_** cell.
3. This cell now enters the bloodstream and looks for signs of **inflammation**, at which point it enters the tissue.
4. The cell is now activated by a **_macrophage_** and begins releasing cytokines.
5. **Eosinophils** follow the cytokines to the area.
32
Delayed hypersensitivity:
1. Allergen is sensed in skin by a **dendritic** cell.
2. The above cell travels to a __________ where it activates a **TH2** cell.
3. This cell now enters the bloodstream and looks for signs of \_\_\_\_\_\_\_\_\_\_, at which point it enters the tissue.
4. The cell is now activated by a **macrophage** and begins releasing cytokines.
5. __________ follow the cytokines to the area.
Delayed hypersensitivity:
1. Allergen is sensed in skin by a **dendritic** cell.
2. The above cell travels to a **_lymph node_** where it activates a **TH2** cell.
3. This cell now enters the bloodstream and looks for signs of **_inflammation_**, at which point it enters the tissue.
4. The cell is now activated by a **macrophage** and begins releasing cytokines.
5. **_Eosinophils_** follow the cytokines to the area.
33
How long does a delayed hypersensitivity reaction (type IV HSR) typically take to manifest?
24 - 48 hours
34
Are antihistamines effective at mediating type IV hypersensitivity?
**No**
35
**True/False**.
Delayed (type IV; cytotoxic) hypersensitivity is mediated by CD8 T cells and mast cells _only_.
**False**.
Delayed (type IV; cytotoxic) hypersensitivity ***responses are all mediated by T cells*** (*the type varies with infectious agent*).
36
TH1 cells _mainly_ activate what cell type(s)?
TH2 cells _mainly_ activate what cell type(s)?
TH17 cells _mainly_ activate what cell type(s)?
**Macrophages** & **TC cells** (pain, inflammation)
**Eosinophils** & **B cells** (itch, allergic inflammation)
**Neutrophils** (pain, pyogenic inflammation)
37
TH1 cells _mainly_ activate what cell type(s)?
**Macrophages** & **TC cells** (pain, inflammation)
38
TH2 cells _mainly_ activate what cell type(s)?
**Eosinophils** and **B cells** (itch, allergic inflammation)
39
TH17 cells _mainly_ activate what cell type(s)?
**Neutrophils** (pain, pyogenic inflammation)
40
Which cytokine is the main inducer for a TH0 cell to become a TH1 cell?
IL-12
41
Which cytokine is the main inducer for a TH0 cell to become a TH2 cell?
IL-4
42
Which cytokines are the main inducers for a TH0 cell to become a TH17 cell?
IL-6, TGF-β
43
Which cytokine is the main inducer for a TH0 cell to become a TReg cell?
TGF-β
44
TH1 cells _mainly_ activate macrophages and TC cells in response to what infection type(s)?
TH2 cells _mainly_ activate eosinophils and B cells in response to what infection type(s)?
TH17 cells _mainly_ activate neutrophils in response to what infection type(s)?
**Viruses** (pain, inflammation)
**Helminths, ticks, mites** (itch, allergic inflammation)
**Bacteria** (pain, pyogenic inflammation)
45
PPD testing mainly involves T\_\_\_ cells.
PPD testing mainly involves TH**1** cells.
46
Allergic dermatitis mainly involves T\_\_\_ cells.
Allergic dermatitis mainly involves T**H2** cells.
47
Autoinflammation mainly involves T\_\_\_ cells.
Autoinflammation mainly involves T**H17** cells.
48
An individual who has no pre-sensitization / previous immune experience with mosquitoes is bitten by one.
Can this individual undergo a type I hypersensitivity reaction?
Why or why not?
**No**.
No IgE for mast cells has been produced yet as no B cell maturation has occurred as the the antigen has not been encountered before.
49
Mast cell degranulation releases **histamine**, **serotonin**, **heparin**, **eosinophilic** **chemotactic** **factors**, \_\_\_\_\_\_\_ase, leukotriene \_\_\_, prostaglandin \_\_\_, IL-\_\_\_, and **TNF-α**.
Mast cell degranulation releases **histamine**, **serotonin**, **heparin**, **eosinophilic** **chemotactic** **factors**, **_trypt_**ase, leukotriene **_C4_**, prostaglandin **_D2_**, IL-**_4_**, and **TNF-α**.
50
Why do degranulating mast cells release IL-4?
To promote TH2 cells and IgE production
51
Why do degranulating mast cells release PGD2?
Strong chemokine for **eosinophils**, **basophils**, and **TH2** cells
52
Why do degranulating mast cells release leukotriene C4?
Increased vascular permeability and bronchoconstriction
53
**True/False**.
Eosinophils are one of the most toxic and destructive cell types in the body.
True.
54
Name the cell type that can synthesize and release all the following:
**Pre-formed**: Major basic protein, _(name of cell)_ cationic protein, _(name of cell)_-derived neurotoxin, _(name of cell)_ peroxidase
**On-demand**: IL-1, IL-2, IL-4, IL-5, IL-6, IL-8, IL-13, TNF-α
**Eosinophils**
**Pre-formed**: Major basic protein, eosinophil cationic protein, eosinophil-derived neurotoxin, eosinophil peroxidase
**On-demand**: IL-1, IL-2, IL-4, IL-5, IL-6, IL-8, IL-13, TNF-α
55
Where do mast cells get their IgE?
From pre-sensitized plasma cells
56
Describe how _immediate_ allergic reactions may change in response to the following levels of interaction with an antigen:
## Footnote
**No previous contact**
**Few previous encounters**
**Multiple previous encounters**
**Very many previous encounters**
57
Describe how _delayed_ allergic reactions may change in response to the following levels of interaction with an antigen:
## Footnote
**No previous contact**
**Few previous encounters**
**Multiple previous encounters**
**Very many previous encounters**
58
\_\_\_\_\_\_\_\_\_\_\_ released from mast cells causes _itching_ by its action on \_\_\_\_\_\_\_\_\_\_\_\_.
\_\_\_\_\_\_\_\_\_\_\_ released from mast cells causes _edema_ by its action on \_\_\_\_\_\_\_\_\_\_\_\_.
**Histamine** released from mast cells causes _itching_ by its action on **C fibers**.
**Histamine** released from mast cells causes _edema_ by its action on **venules**.
59
Why do we have an itch-scratch reflex mediated by the histamine released during an _immediate_ reaction?
Does this reflex involve the brain at all?
To attempt to **remove any noxious stimuli** (e.g. ticks or substances) from the skin;
**no**
(dogs with severed spinal cords will still scratch at noxious stimuli)
60
How long does a Ixodes tick take to infect someone with *Borrelia burgdorferi*?
~24 hours
(about 24 hours until sufficient engorgement for backwash to occur)
61
Why do we have an itch-scratch reflex mediated by the histamine released during a _delayed_ reaction?
To attempt to **remove infected skin** so the damaging substance doesn't enter the bloodstream
(literally removing damaged/diseased flesh)
62
Most *clinical* cases of hypersensitivity are either classified as _____________ hypersensitivity or _____________ hypersensitivity.
Most *clinical* cases of hypersensitivity are either classified as **_immediate_** hypersensitivity or **_delayed_** hypersensitivity.
63
What antibody class mediates tissue glutaminase destruction in Celiac disease?
IgA
64
Why can antigens be immunogenic if taken up through the skin and tolergenic if taken up orally?
65
What is **eradication** in terms of infectious disease?
What is **elimination** in terms of infectious disease?
Complete and permanent reduction to zero of new cases from the disease _worldwide_.
Complete and permanent reduction to zero of new cases from the disease _in a defined geographic area_.
66
What are homologous antibodies?
And heterologous?
Human-derived;
synthetic or animal-derived
67
Against which of the following types of infectious agent do we develop vaccines?
**Bacteria**
**Fungi**
**Parasites**
**Viruses**
**Bacteria**
**Viruses**
(simpler, less complex infectious agents)
68
What are the two main subtypes of killed/inactivated vaccines?
1. **Whole**
2. **Fractional**
69
Fractional killed vaccines can be broken down into two subcategories based on what type of material they bind, \_\_\_\_\_\_\_-based or \_\_\_\_\_\_\_-based.
Fractional killed vaccines can be broken down into two subcategories based on what type of material they bind, **protein**-based or **polysaccharide**-based.
70
What are the subtypes of protein-based killed vaccine?
And polysaccharide-based?
Toxoid, subunit;
pure, conjugated
71
What type of vaccine typically only requires **one dose** to create strong, lasting immunity?
Live attenuated
72
**True/False**.
The infectious agent in a live attenuated vaccine must replicate a bit in order to induce immunity (basically a mini-infection).
True.
73
# Fill in the blanks regarding vaccine types:
I. **Whole**
A. Viral or \_\_\_\_\_\_\_\_
II. **Fractional**
A. Protein-based
1. \_\_\_\_\_\_\_
2. \_\_\_\_\_\_\_
B. \_\_\_\_\_\_\_-based
1. Pure
2. \_\_\_\_\_\_\_
## Footnote
I. **Whole**
A. Viral or _bacterial_
II. **Fractional**
A. Protein-based
1. _Subunit_
2. _Toxoid_
B. *Polysaccharide*-based
1. Pure
2. *Conjugated*
74
Why doesn't the U.S. provide the BCG vaccine to its citizens?
So PPD tests remain accurate methods of determining who's been infected and who hasn't
(also, cost)
75
Why do children receive multiple rounds of vaccines?
Affinity maturation / class switching
(better immune responses with more exposures)
76
Is it better to have a shorter (few weeks) or longer (few months) break between repeat dosages of a vaccine?
**_Longer_**
(time for immune response maturation --- affinity maturation, class switching, etc.)
(better late than too early)
77
Who are the most at-risk groups for adverse reactions to vaccines?
Neonates;
the immunocompromised;
the elderly
78
What are a few contraindications to live vaccines?
Pregnancy;
prior severe allergic response;
certain immunocompromising conditions
79
Where can a physician get better information as to when to give vaccines, which to give, and what the contraindications are?
The **CDC** **website**
| (updated very frequently)
80
What is the most common adjuvant used in vaccination?
What is the purpose of adjuvants?
**Aluminium**;
to induce **inflammation**
(thus boosting the immune response)
81
What can we measure in an individual to make sure a vaccine worked as intended?
Serum IgG
82
What type of vaccine is the MMR?
Live attenuated
83
What type of vaccine is the BCG?
Live attenuated
| (bacterial)
84
What type of vaccine is the oral typhoid vaccine?
Live attenuated
| (bacterial)
85
What type of vaccine is the hepatitis B vaccine?
Subunit
| (subtype of inactivated/killed)
86
What type of vaccine is the diphtheria vaccine?
Toxoid
| (subtype of killed/inactivated)
87
What type of vaccine is the *H. influenzae* vaccine?
Conjugate-polysaccharide
(subtype of killed/inactivated)
88
What type of vaccine is the Salk polio vaccine?
Killed/inactivated
| (whole virus)
89
What type of vaccine is the Sabin polio vaccine?
Live attenuated
90
What type of vaccine is the hepatitis A vaccine?
Killed/inactivated
| (whole virus)
91
What type of vaccine is the nasal influenza vaccine?
Live attenuated
92
What type of vaccine is the meningococcal vaccine?
EITHER
pure- or conjugate-polysaccharide
(subtype of killed/inactivated)
93
What type of vaccine is the injected influenza vaccine?
Killed/inactivated
| (whole virus)
94
What type of vaccine is the rabies vaccine?
Killed/inactivated
| (whole virus)
95
What type of vaccine is the acellular pertussis vaccine?
Subunit
| (subtype of killed/inactivated)
96
What type of vaccine is the pneumococcal vaccine?
EITHER
pure- or conjugate-polysaccharide
(subtype of killed/inactivated)
97
What type of vaccine is the rotavirus vaccine?
Live attenuated
98
What type of vaccine is the anthrax vaccine?
Subunit
| (subtype of killed/inactivated)
99
What type of vaccine is the HPV vaccine?
Subunit
| (subtype of killed/inactivated)
100
What type of vaccine is the yellow fever vaccine?
Live attenuated
101
What type of vaccine is the tetanus vaccine?
Toxoid
| (subtype of killed/inactivated)
102
What type of vaccine is the Herpes zoster vaccine?
Live attenuated
103
What type of vaccine is the varicella vaccine?
Live attenuated
104
What four killed/inactivated vaccines for bacterial agents are not available in the U.S.?
And what one live attenuated vaccine for a bacterial agent?
Cholera, pertussis, typhoid, plague;
BCG
105
The ____________ event is the initial event leading to dysregulated cell growth and potential proliferation / tumor growth.
The **_transformation_** event is the initial event leading to dysregulated cell growth and potential proliferation / tumor growth.
106
**True/False**.
Cancer cells grow independently of density.
**True**.
May lead to a necrotic center as the center is starved of nutrients.
107
Name a few selective forms of cancer treatment.
**Gene** therapy,
**targeted** therapy,
**immuno**therapy
108
**True/False**.
Most tumors are not immunogenic as they are self cells.
**False**.
Often, tumors have immunogenicity, they just grow faster than the immune system can keep up.
109
Are tumor vaccines useful before or after tumor growth or both?
**Before _only_**
(only helpful prophylactically, but nobody knows about the tumor until after it already exists)
110
What cell type is the main mediator of the cellular anti-tumor immune response?
TC cells
| (TH cells assist)
111
What cell type is the main innate immune response to tumor cells?
What role do macrophages play?
**NK** cells;
**TNF-α** (cachexin) secretion
112
Why are natural killer cells such a big part of the body's response to tumor cells?
Tumor cells often **downregulate MHC I**
113
\_\_\_\_\_\_\_\_\_\_\_ immunity --- a type of immunity in which the body prevents **secondary** tumors from growing while being unable to contain the **primary** tumor (anti-metastases).
**_Concomitant_** immunity --- a type of immunity in which the body prevents **secondary** tumors from growing while being unable to contain the **primary** tumor (anti-metastases).
114
**Concomitant** immunity --- a type of immunity in which the body prevents __________ tumors from growing while being unable to contain the __________ tumor (anti-metastases).
**Concomitant** immunity --- a type of immunity in which the body prevents **_secondary_** tumors from growing while being unable to contain the **_primary_** tumor (anti-metastases).
115
Tumors often recruit _______ to **downplay** the immune response.
Tumors often recruit **TRegs** to **downplay** the immune response.
116
The following two mutations can result in tumor-_specific_ antigens:
## Footnote
(**1**) mutation in _______ to hold new protein
(**2**) mutation in original MHC-bound _______ to form new epitope
The following two mutations can result in tumor-_specific_ antigens:
## Footnote
(**1**) mutation in **_MHC I_** to hold new protein
(**2**) mutation in original MHC-bound **_protein_** to form new epitope
117
The following two mutations can result in tumor-_associated_ antigens:
(**1**) Reactivation of ________ genes
(**2**) Overexpression of ________ proteins
The following two mutations can result in tumor-_associated_ antigens:
(**1**) Reactivation of **_embryonic_** genes
(**2**) Overexpression of **_self_** proteins
118
\_\_\_\_\_\_\_\_\_ (mutated protooncogenes) are like an overactive gas pedal.
How many are needed to cause excessive growth and tumor formation?
**_Oncogenes_** (mutated protooncogenes) are like an overactive gas pedal.
**One** (one gas pedal)
119
Inactivated _________ \_\_\_\_\_\_\_\_\_ genes are like a broken car brake.
How many are needed to cause excessive growth and tumor formation?
Inactivated **tumor suppressor** genes are like a broken car brake.
**Two** (the handbrake and the brake pedal)
120
Cancer defenses against immunity are often mediated by de-differentiation to \_\_\_\_\_\_\_, more \_\_\_\_\_-cell-like forms.
Cancer defenses against immunity are often mediated by de-differentiation to **_immature_**, more **_stem_**-cell-like forms.
121
Cancer defenses against immunity are often mediated by de-differentiation to immature, more stem-cell-like forms:
## Footnote
**1**. Low immunogenicity (downregulated \_\_\_\_/peptide; absence of co-stimulation for self-antigens --\> _______ of T cells; no _______ molecules; absence of inflammation)
**2**. Recruiting Tregs
**3**. Antigenic modulation --- antibody binding surface antigen leads to endocytosis and destruction of antigen by tumor cell
**4**. Immunoediting --- selective changes in expressed antigens
**5**. Creation of a physical barrier to immune activity (encapsulation)
Cancer defenses against immunity are often mediated by de-differentiation to immature, more stem-cell-like forms:
## Footnote
**1**. Low immunogenicity (downregulated **_MHC_**/peptide; absence of co-stimulation for self-antigens --\> **_anergy_** of T cells; no **_adhesion_** molecules; absence of inflammation)
**2**. Recruiting Tregs
**3**. Antigenic modulation --- antibody binding surface antigen leads to endocytosis and destruction of antigen by tumor cell
**4**. Immunoediting --- selective changes in expressed antigens
**5**. Creation of a physical barrier to immune activity (encapsulation)
122
Cancer defenses against immunity are often mediated by de-differentiation to immature, more stem-cell-like forms:
## Footnote
**1**. Low immunogenicity (downregulated MHC/peptide; absence of co-stimulation for self-antigens --\> anergy of T cells; no adhesion molecules; absence of inflammation)
**2**. Recruiting \_\_\_\_\_
**3**. Antigenic modulation --- antibody binding surface antigen leads to _______ and destruction of antigen by tumor cell
**4**. Immunoediting --- selective changes in expressed antigens
**5**. Creation of a physical barrier to immune activity (encapsulation)
Cancer defenses against immunity are often mediated by de-differentiation to immature, more stem-cell-like forms:
## Footnote
**1**. Low immunogenicity (downregulated MHC/peptide; absence of co-stimulation for self-antigens --\> anergy of T cells; no adhesion molecules; absence of inflammation)
**2**. Recruiting **_Tregs_**
**3**. Antigenic modulation --- antibody binding surface antigen leads to **_endocytosis_** and destruction of antigen by tumor cell
**4**. Immunoediting --- selective changes in expressed antigens
**5**. Creation of a physical barrier to immune activity (encapsulation)
123
Cancer defenses against immunity are often mediated by de-differentiation to immature, more stem-cell-like forms:
## Footnote
**1**. Low immunogenicity (downregulated MHC/peptide; absence of co-stimulation for self-antigens --\> anergy of T cells; no adhesion molecules; absence of inflammation)
**2**. Recruiting Tregs
**3**. Antigenic modulation --- antibody binding surface antigen leads to endocytosis and destruction of antigen by tumor cell
**4**. Immunoediting --- selective changes in expressed \_\_\_\_\_\_\_\_\_\_
**5**. Creation of a _________ barrier to immune activity (en\_\_\_\_\_lation)
Cancer defenses against immunity are often mediated by de-differentiation to immature, more stem-cell-like forms:
## Footnote
**1**. Low immunogenicity (downregulated MHC/peptide; absence of co-stimulation for self-antigens --\> anergy of T cells; no adhesion molecules; absence of inflammation)
**2**. Recruiting Tregs
**3**. Antigenic modulation --- antibody binding surface antigen leads to endocytosis and destruction of antigen by tumor cell
**4**. Immunoediting --- selective changes in expressed **_antigens_**
**5**. Creation of a **_physical_** barrier to immune activity (en**_capsu_**lation)
124
Immune reaction to a tumor cell often __________ over time.
Immune reaction to a tumor cell often **_decreases_** over time *(tumor cells adapt)*.
125
How can specific tumor immunogenicity be tested?
It can't
126
Tumor vaccines can be used to immunize an individual with tumor-\_\_\_\_\_\_\_-pulsed (or \_\_\_\_-transfected) dendritic cells.
However, they are not useful ______ the tumor has already formed.
Tumor vaccines can be used to immunize an individual with tumor-**_antigen_**-pulsed (or **_DNA_**-transfected) dendritic cells.
However, they are not useful **_after_** the tumor has already formed.
127
Anticancer cytokine therapy is typically designed to increase immune response to what?
Cytokines
| (e.g. IL-2, GM-CSF, IL-12, etc.)
128
How does passive anticancer immunotherapy work?
Removal / expansion / readministration of a patient’s own T cells
129
Monoclonal antibodies against breast cancer often target what tumor-specific antigen?
HER-2/NEU
130
Monoclonal antibodies against B cell lymphomas often target what tumor-specific antigen(s)?
CD20,
CD10
131
Monoclonal antibodies against GI and lung cancers often target what tumor-specific antigen(s)?
CEA
132
Monoclonal antibodies against ovarian cancers often target what tumor-specific antigen(s)?
CA-125
133
Monoclonal antibodies against melanoma often target what tumor-specific antigen(s)?
CD3 ganglioside
134
Name two **anticancer** **immunotherapies** that target T cell inhibition receptors in order to **increase** T cell activity.
Anti-\_\_\_\_\_\_\_ therapy;
anti-\_\_\_\_\_\_\_ therapy
Anti-**PD-1** therapy;
anti-**CTLA-4** therapy
*(both to inhibit T-cell-inhibiting activity)*
135
Treg cells that express FoxP3 are generally thought to have T-cell receptors that recognize self-peptides bound to MHC class II molecules. In the skin, keratin and filaggrin are among the self-antigens expressed. FoxP3+ Treg cells found in skin and skin-draining lymph nodes might be specific for the self-antigen, filaggrin.
**These FoxP3+, filaggrin-specific Treg cells:**
A. Would inhibit the activation of both naive filaggrin-specific and keratin-specific CD4 T cells
B. Would only inhibit the activation of naive filaggrin-specific CD4 T cells
C. Would inhibit the activation of all naive T cells in skin-draining lymph nodes following an infection
D. Would not inhibit naive T cells specific for antigens expressed by commensal microbes but not by host cells
E. Are the only subset of autoreactive cells expressing TGF-b receptors
A. Would inhibit the activation of both naive filaggrin-specific and keratin-specific CD4 T cells
## Footnote
**Treg cells have the potential to suppress self-reactive lymphocytes that recognize antigens different from those recognized by the Treg cell. The key feature is that regulatory cells can suppress autoreactive lymphocytes that recognize a variety of different self-antigens, as long as the antigens are from the same tissue or are presented by the same antigen-presenting cell.**
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Bacteria of the genus Neisseria are encapsulated in a thick carbohydrate capsule. Clinical evidence shows that the membrane-attack complex (MAC) is vital in host defense against these bacteria. It is obvious that the hydrophobic components of the MAC cannot penetrate the polysaccharides of the bacterial capsule. **How, then, is complement involved in bacterial killing in this case?**
The bacteria are **temporarily** **vulnerable** to killing by complement **when** **they** **divide**.
This is when the bacterial membrane is exposed.
