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PRIN > PRIN 14 Immunity > Flashcards

PRIN 14 Immunity Flashcards

1
Q

TH1 vs TH2

A

TH1: help activate macrophages
(role in Cell mediated Imm)

TH2: help activate naive B cells
(role in Humoral Imm)

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2
Q

Describe TCR Structure

A

a chain & b chain

both attached to a V and C region

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3
Q

What is the purpose of Positive Selection?

A

Choosing T cells that recognize peptide Ags

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4
Q

What is the purpose of Negative Selection?

A

Eliminating T cells that recognize TOO strongly to self Ag

prevent autoimmunity

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5
Q

What is needed to stimulate T Cells to proliferate and differentiate?

A

(1) Ag recognition
(2) Costimulation
(3) Cytokines

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6
Q

How does a CTL destroy target cells?

A

CTL binds DIRECTLY to target cell
Delivers Perforin & Granzyme B into the cell

Granzyme B triggers Caspases …apoptosis

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7
Q

What are TH17 cells?

A

Secrete IL-17 & IL-22

Host defense against bacterial & fungal infections

Role in tissue inflammation during autoimmunity

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8
Q

What is the role of T Regulatory cells?

A

Block activation of harmful lymphocytes specific for self Ag

Protect self from autoimmunity

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9
Q

Example of T cell role in Communicable Disease

A

People who have had TB develop memory T cells specific for TB Ags.

Therefore, when tested with SC injection … strong response

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10
Q

Example of T cell role in Non-communicable Disease

A

Obesity / Diabetes / Cancer

Islet Specific T cells in Type 2 DM secrete altered levels of cytokines. Changes occur in adipose, liver, pancreatic islets, vasculature

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11
Q

During the course of ones life, when does B cell production occur?

A

Begins before birth and continues throughout lifetime

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12
Q

Describe structure of Ig…

A

Light & Heavy Chains (Fab) with a constant (Fc) region at base.

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13
Q

What mechanisms contribute to the generation of Ig diversity?

A

(1) Combination of multiple gene segments (VDJ)
(2) Pairing of H & L Chains
(3) Junctional Diversity (addition / deletion of DNA bases)
(4) Somatic Hypermutation

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14
Q

What is Somatic Hyoermutation?

Which cells undergo it?

A

High rate of point mutations within VDJ gene DNA

Stimulated by cytokine signals via TH cells

Additional mutation occurring AFTER mature B cells are activated

Affects B cells ONLY

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15
Q

What is Anergy?

A

State of being non-functional

Unresponsive to Ag

Ag is there … but lack of cytokines mean no reactivity by B cells

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16
Q

Where do B cells go after they mature and leave the bone marrow?

A

Secondary Lymphoid Organs:

  • Spleen
  • Lymph Nodes
  • Tonsils
  • GALT & MALT
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17
Q

What happens during a T-Independent Ag response?

A

Involves Carbs / lipid Ag ..

(1) B-cell BCRs cluster via repeating carb units on microbe
(2) B Cell PRR responds to PAMP on microbe

RESULT: B cells proliferate and differentiate into Ab secreting cells (but NO memory cells)

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18
Q

Provide an example of surface interactions that occur during T-dependent activation of B-cells

A

Protein interactions between TH cell and B-cell

T-Cell CD28 binds to B-Cell B7

T-Cell CD40L binds to B-Cell CD40

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19
Q

What is required for Isotype class switching?

A

Must have the interaction between:

(1) T-Cell CD40L binds to B-Cell CD40
(2) Cytokines

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20
Q

What directs Isotype switching?

A

Cytokines

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21
Q

What happens if an individual has a mutation in CD40L?

A

T-Cell CD40L binding to B-Cell CD40
WILL NOT OCCUR

Therefore, this ppt will be stuck at IgM

RESULT: X-Linked hyper IgM syndrome

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22
Q

Order of Ig Production

A

MDGEA

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23
Q

What do secreted Abs do?

A

(1) coat infected cell, promoting NK attack
(2) Complement Activation
(3) Opsonization
(4) Neutralization

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24
Q

Which Ig is the greatest in the blood?

A

IgG

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25
Q

IgG Characteristics

A

Can cross placenta

Predominant IgG in blood

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26
Q

IgA Characteristics

A

Resistant to stomach acid
protects mucosal surfaces
secreted in milk

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27
Q

IgM Characteristics

A

FIRST Ab produced
Pentamer (so its big)
NOT CROSS PLACENTA

28
Q

IgE Characteristics

A

Defends against parasites

causes allergies

29
Q

What is PID?

A

Primary Immune Deficiency

  • Genetically determined
  • Enhanced susceptibility to infectious disease, autoimmunity and malignancy
30
Q

What are current treatment options for primary immunodeficiency?

A

(1) Passive admin of Abs
(2) Prophylactic Abx
(3) Stem Cell transplantation
(4) Gene Therapy

31
Q

What are Secondary Immune Defiencies?

A

ACQUIRED

(eg) HIV, Malnutrition, Medically induced immunosuppression

32
Q

Gel & Coombs Classification of Hypersensitivities

A

(1) IgE mediated H.
(2) Ab mediated H.
(3) Immune Complex mediated H.
(4) Cell Mediated H. (time delayed)

33
Q

Gel & Coombs Classification of Hypersensitivities

TYPE 1

A

(1) IgE mediated H.
ALLERGIES
IgE for specific Ag is produced and then sits on Mast Cells … gets activated

Wheel >2mm indicates IgE production for specified Ag

34
Q

What is the new way to treat Allergic Diseases?

A

DRUG: Omalizumab
Anti-IgE Ab: approved in Canada for severe asthma (expensive)
Recognizes IgE and takes it out of circulation

35
Q

Gel & Coombs Classification of Hypersensitivities

TYPE 2

A

(2) Ab mediated H.
Abs target self Ags and trigger destruction of self cells (autoimmune)

(eg) Blood Type Rejection
(eg) Hemolytic Disease of Newborn

36
Q

Gel & Coombs Classification of Hypersensitivities

TYPE 3

A

(3) Immune Complex mediated H.

Immune Complexes form and get deposited in small vessels and in joints … cause inflammation
(eg) SLE, Serum Sickness

37
Q

Is SLE considered a Primary Immune Disease?

A

No, SLE is not conferred by a single gene. There is myriad of variable factors that contribute to the disease.
(genetics AND environment)

Note .. Lupus is actually Types 2 & 3

38
Q

Diagnosing SLE

A 
4/7:
Rash
Discoid Rash
Photosensitivity
Oral Ulcers
Arthritis
Serositis
Kidney dysfunction
CNS involvement ... seizures
Cytopenia
Immunologic tests
Antinucelar Abs
39
Q

Gel & Coombs Classification of Hypersensitivities

TYPE 4

A

(4) Cell Mediated H. (time delayed)

CD4 TH cells can activate macrophages or eosinophils
CD8 CTLs cause tissue damage

often takes several days to set in

40
Q

Examples of Type 4

A

(4) Cell Mediated H. (time delayed)

Contact Dermatitis
Mantoux Test / TB test
Type 1 DM
MS

41
Q

What are the 3 signals from the Innate APC required to induce Adaptive Immunity?

A

(1) Ag Presentation
(2) Co-stimulation
(3) Cytokines

42
Q

What is the role of cytokines?

A

Steer / direct / shape the quality & quantity of the immune response.
Cytokines are involved in the specific differentiation of T cells in proliferation

43
Q

What states do Lymphocytes need to be in to exert effector functions?

A

Must be activated to offer protection from infection

Naive Adaptive Cells do NOT protect

44
Q

What are the three “tempos” of immune response?

A

(1) RAPID
Immediate
Innate

(2) INTERMEDIATE
5-7 days
Innate & Adaptive
(most disease for vaccines)

(3) SLOW
>7 days
Adaptive
(most infections are cleared without us even knowing they were ever there…)

45
Q

What are examples of pathogen virulence within the 3 tempos?

A

(1) RAPID
Ebola v

(2) INTERMEDIATE
Pneumococcus
Influenza

(3) SLOW
M. Tuberculosus
H. Papillomavirus

46
Q

What are the 4 steps in Lymphocyte action?

A 
Selection
Activation
Expansion
Contraction
(>95% of Ag specific immune cells die ... only a few are retaiend as memory)
47
Q

How are Memory Cells stimulated?

A

Only need Antigen to be presented

**do not need (2) Costimulation and (3) cytokines

48
Q

Vaccines prevent infections by …

A

Vaccines prevent infections by …

…inducing protective immune memory

49
Q

What is Arepanrix (GSK)

A 
Trade name Flu Shot
(1) Antigen: influenza v. inactivated
(2) Adjuvent:
a-tocopherol (Vit E)
Squalene
50
Q

Why is a-tocopherol used?

A

Vit E

lipid based - keeps squalene in solution

51
Q

Why is squalene used?

A

Main adjuvent

Causes inflammation via disruption of cell membrane

52
Q

What else is a good adjuvent

A

Aluminum

53
Q

Why use adjuvents? How do they make vaccines work?

A

Adjuvents work by upregulating

(2) costimulation
(3) cytokines

54
Q

What does a Positive Hep C test indicate?

A

she been previously exposed to Hep C
OR
has a chronic HepC infection

55
Q

In the Hep C pregnant woman, the rash on ther legs is caused by which type of Hypersensitivity Reaction?

A

Type 3: Immune Complex Mediated Hypersensitivity

56
Q

Why did the doctor ask if Concepion had any joint pain?

A

To assess if the immune complexes were getting deposited in her joints. This occurs in about 1/3 of Hep C patients.

57
Q

Hemolytic Disease of Newborn is caused by what type of Hypersensitivity Reaction?

A

Type 2 Ab mediated Hypersensitivity.

58
Q

How does RF connect with this case?

A

In 1/3 of Hep C cases, IgM will be evoked to bind the Fc region of the IgG-Hep C complex. This will result in BIG ASS immune complex forming and getting deposited in small vessels.

59
Q

In a male with O negative blood what Abs would be in his serum?

A

anti-A and Anti-B only

(he’s never encountered Rh(D) in order to produce Abs / memory against it

60
Q

How do CTL’s kill?

A

Once in direct contact with affected cell, CTL releases Perforin & Granyme B into it … triggers Caspases … apoptosis

61
Q

What is the affect of a patient having no CD40 ligand on the surface of his T cells?

A

Isotype / Class Switching cannot occur

62
Q

What is Arthralgia?

A

Joint Pain

63
Q

Arthralgia is an example of which Gel & Coombs Hypersensitivity?

A

Type 3 Hypersensitivity: Immune Complex

64
Q

When immune complexes deposit on blood vessel endothelium in the skin, a rash may develop. The damage to the blood vessels at the site of IC deposition is predominantly mediated by which of the following activated cells or systems?

A

Neutrophils

65
Q

A woman with blood type A+ is pregnant for the first time with a fetus that has B+ blood. Why DOESNT the woman destroy the fetal red cells?

A

Maternal antibodies to blood ABO proteins are typically IgM.

PRIN (13 decks)

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