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Immunology 2019 > Lecture 22 > Flashcards

Lecture 22 Flashcards

1
Q

Categorize the 4 types of Hypersensitivity in terms of what type of pathogens they attack (extra or intracellular) and what mediates them.

A

Types I, II, and III attack Extracellular pathogens
These are Ab-mediated immune responses

Type IV attack Intracellular pathogens
This is a Cell-mediated immune response

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2
Q

For the 4 types of Hypersensitivity, briefly describe their cause/mechanism

A

Type I: caused by the actions of inflammatory mediators for MAST cells

Type II: caused by Abs against cell/tissue Ags

Type II: caused by Abs against Circulating Ags (causes vasculitis due to immune complexes depositing in vessels)

Type IV: T cell-mediated response

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3
Q

For type IV hypersensitivity, state the 3 T cells that are involved and the roles they play

A

Th1 cells: produce inflammatory cytokines

Th17 cells: produce inflammatory cytokines

CTLs: kill host cells

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4
Q

Why hypersensitivity type is associated with allergic reactions? what specific Ig class of Ab causes this and what cells produce it?

A

Type I hypersensitivity

IgE from Mast cells and Th2 cells

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5
Q

Define Atopy. Include the main characteristic of a reaction that classifies it as atopic.

A

Atopy: genetic tendency to develop allergic diseases

Atopic responses are UNUSUALLY aggressive reactions to an UNUSUALLY SMALL amount of Ag

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6
Q

In Type I reactions, IgE Abs have a high affinity for ____ on the membrane of what 3 cell types?

A

FcSigmaR1

Mast cells, Basophils, Eosinophils

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7
Q

Describe the 1st and 2nd encounter with an Ag that causes a Type I hypersensitivity reaction

A

1st encounter:
The Ag binds to B cells, which activate Th2 cells to produce IgE
This IgE then binds to the FcSigmaRI on the surface of mast cells (priming the mast cells)
There is NO immune reaction however

2nd encounter:
The Ag binds to the IgE-FcSigmaRI on the surface of the mast cells, activating them to release mediators
There IS a hypersensitivity reaction

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8
Q

The following mediators are involved in what type of hypersensitivity reaction? Which of these are preformed and stored in granules so that they may be quickly released when needed?

Histamine
Proteases
Prostaglandins
Leukotrienes
Cytokines
A

Are all type I mediators

Histamine and Proteases are preformed and stored in granules

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9
Q

Describe the effect of the following mediator. Explain how this causes edema.

Histamine

A

Histamine: Dilates blood vessels in order to increase vascular permeability

Histamine causes edema by increasing the vascular pressure via local dilation of blood vessels and tightening the downstream vessels
(Histamine has a different affect as it is metabolized. Dilates initially, constricts after it has spent time being metabolized by the body)

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10
Q

Describe the effect of the following mediator.

Proteases

A

Proteases: Damage local tissues

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11
Q

Describe the effect of the following mediator.

Prostaglandins

A

Prostaglandins: Vascular dilation

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12
Q

Describe the effect of the following mediator.

Leukotrienes

A

Leukotrienes: cause prolonged smooth muscle contraction

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13
Q

Describe the effect of the following mediator during a type I hypersensitivity response.

Cytokines

A

Cytokines: cause “late phase” local inflammation

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14
Q

State the hallmarks of immediate hypersensitivity.

A

(immediate hypersensitivity = Type I hypersensitivity)

Acute vascular reactions, smooth muscle reactions, and inflammation

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15
Q

During a type I hypersensitivity reaction, compare the immediate and late phases of the reaction in terms of the time after exposure it occurs and the characteristics of the reaction

A

Immediate Phase: occurs within minutes of exposure
Vascular and smooth muscle reactions (cause Vasodilation, Congestion, and Edema)

Late Phase: occurs 2-24 hrs after exposure
Eosinophils, Neutrophils, and T cell levels are elevated

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16
Q

Asthma is a _____ airway obstruction that is an example of type ___ hypersensitivity

A

Reversible

Type I

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17
Q

What 2 characteristics of asthma contribute most to the constriction of the airway?

A

Increased capillary permeability

Spasmodic contraction of the smooth muscle surrounding the bronchioles

(these both decrease the size of the bronchial lumen and cause SOB)

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18
Q

State 3 non-immunologic stimuli that are known to cause asthma. (one of these is tricky)

A

Cold

Viral infections

Exercise

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19
Q

Chronic _____ use can lead to a desensitization that can lead to asthma

A

steroid

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20
Q

What is released in order to trigger an anaphylactic reaction to an Ag? State the 2 characteristics that best describe an Anaphylaxis reaction and what this does to BP.

A

Rapid release of vasoactive amines (from mast cells/basophils)

  1. Contraction of smooth muscle in vasculature
  2. Vasodilation of capillary endothelium

Greatly decreases BP

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21
Q

Which type of hypersensitivity reaction is anaphylaxis? What is the term used to describe the state of greatly decreased BP a pt experiences during an anaphylactic reaction?

A

Type I

Vascular Shock: state of decreased BP from anaphylactic reactions

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22
Q

When conducting Allergen testing by injecting Ags into the dermis, what do you look for during the test to decide if the pt is allergic to the Ag or not? What side of the arm is this usually conducted on?

A

Positive reactions are indicated as “Redness and swelling within 20-30 minutes”

The ventral side of the arm

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23
Q

What are the 2 characteristics of a Type II hypersensitivity reaction?

A
  1. Abs activate the complement system via the classical (Ab mediated) pathway
  2. Abs binds to Neutrophils and Macrophages to cause a proinflammatory response
24
Q

During a type II hypersensitivity reaction, state where the Ab-Ag complexes are deposited. Then state what occurs to the Abs in these complexes that allows them to activate the complement via the classical pathway.

A

Ab-Ag complexes are deposited in the tissues (cell surfaces)

The Fc receptor of the Ab in the Ab-Ag complex is conformationally changed by Neutrophils/Macrophages so that it may then activate the complement
(this occurs when the Ab is interacting with the Neutrophils/Macrophages in order to cause a proinflammatory response ; they both get something out the exchange)

25
Q

The Ags of which type of hypersensitivity reaction are considered to be “Solid”? Which type is considered to be “Soluble”? Include where both of these Ags bind.

A

Type II: “Solid” Abs
Bind to Ags on cell surfaces (tissue)

Type III: “Soluble” Ab
bind to free floating Ags (usually in the bloodstream)

26
Q

Ischemic damage is associated with what type if hypersensitivity reaction? Why is this, and what parts of the body are especially susceptible to this type of damage?

A

Type III bc the Ab-Ag complexes are formed in the circulating blood and deposited in the blood vessels

Organs with lots of blood flow such as the lungs, kidneys, or liver are especially susceptible to this ischemic damage (for obvious reasons)

27
Q

What is the major mechanism that contributes to the tissue damage caused by Type III hypersensitivity reactions?

A

Classical activation of the complement, forming potentially occluding immune complexes in the blood vessels.

28
Q

State the 2 sources of pro-inflammatory molecules that occur during a type III hypersensitivity reaction.

A

Activation of the complement, releasing proinflammatory C3a and C5a

Inflammatory cells (Neutrophils and Basophils) release Vasoactive Amines that cause inflammation

29
Q

State the 4 mechanisms of Type III hypersensitivity reactions that cause tissue damage

A
  1. Mast cell degranulation
  2. Complement activation
  3. Inflammation caused by immune cells
  4. Neutrophil chemotaxis

(“Mast Cell InflammatioN” mnemonic with important letters capitalized)

30
Q

Describe what an Arthus reaction is

A

Arthus Reaction: Subcutaneous injection of a protein Ag to a previously immunized person to measure the level of immune response that occurs
(ex. TB test bubble)

31
Q

SLE, Serum Sickness, and Arthus reactions are all examples of what kind of Hypersensitivity reaction? what are all of these mediated by?

A

Type III

All are mediated by Complement-mediated and Fc receptor-mediated inflammation

32
Q

Compare passive immunization and Serum Sickness

A

Passive immunization: Injecting anti-serium Ags into a pt to assist their immune system (bc their system doesn’t have enough time to develop the necessary Ags)
ex. Administering Rattlesnake antidote

Serum Sickness: occurs if a pt has already been treated via passive immunization of anti-serum Abs and they are give the SAME Abs a 2nd time (since the pt’s body has been exposed to the foreign passive immunization Abs, their immune system will mount an aggressive memory cell reaction to the antidote)
This can be avoided by using antiserums derived from other animals.

33
Q

Which Type of hypersensitivity reaction is associated with chronic inflammation? What cell mediates this type of reaction and what cell causes the tissue damage?

A

Type IV

Th1 (T cells) mediate Type IV reactions

Macrophage activity causes the tissue damage

34
Q

Which type of hypersensitivity reaction is referred to as Delayed type hypersensitivity? Explain why this type cannot be transferred by ONLY serum containing Abs like all of the other types.

A

Delayed type hypersensitivity = Type IV

Type IV hypersensitivity reactions require there to be Ag-specific Th1 clones transferred bc the Th1 cells are what orchestrate the macrophage response (via IFN-gamma production) that characterizes Type IV responses

(all other types can be transferred in serum with ONLY Ag-specific Abs and do not require there to be Th1 clones transferred as well)

35
Q

State the 4 main types of Type IV hypersensitivity autoimmune diseases and state the cells that are damaged by autoimmune T cell activity.

A

MS (multiple sclerosis): Myelin proteins

RA (Rheumatoid Arthritis): Ags in the joint/synovium

Type I diabetes: Beta Langerhan cells in the pancreatic islet

Crohn’s disease: unknown intestinal microbes

36
Q

State the 2 ways that humans can be sensitized for DTH (Delayed-Type Hypersensitivity) reactions caused be microbial infections.

A

Contact sensitization (ex. poison ivy)

Immunization (ex. diphtheria/tetanus toxin vaccines)

37
Q

About how long after exposure does it take for a DTH (Type IV) reaction to occur? why?

A

24-48 hrs

This is about the amount of time that it takes for T cells to be able to proliferate and induce T cell-mediated immune response

38
Q

In a TB granuloma, what 2 cell types usually compose the granuloma? What type of area can usually be found at the middle of the granuloma?

A

Activated Macrophages and Lymphocytes (multinucleate giant cells as well?)

A necrotic area can usually be found in the middle of a granuloma (caused by T cell activity against the granuloma)

39
Q

Explain why TB kills many HIV pts.

A

HIV pt’s have less CD4+ T helper cells than normal pts

When TB forms granulomas in these pt’s, there are not enough strong CD4+ T helper cells to penetrate the Thick outer layer of the granuloma that is formed by a robust Macrophage response
(“Human shield” of macrophages that keeps the TB safe from T cell-mediated destruction)

40
Q

Compare Mature granulomas with granulomas that are newly formed. What type of reactions lead to the formation of Mature granulomas?

A

Mature granulomas successfully build a “macrophage shield” that prevents T cells from contacting and destroying the pathogen

New granulomas are mores susceptible to T cell activity bc they do not have a thick of a “macrophage shield”

“Prolonged Reactions” lead to the formation of mature granulomas

41
Q

During a Type IV hypersensitivity reaction, state the 3 things that cytokines are responsible for.

A
  1. Recruitment of Leukocytes
  2. Activation of Resident Tissue Macrophages
  3. Generation of Th1 cells

“RAG” mnemonic

42
Q

Explain why contact dermatitis type IV reactions to Polysaccharide Ags only occur during the secondary contact with the Ag. (include how long it takes for each part of this to occur)

A

During the 1st encounter with the Ag, the T cells are becoming sensitized to the Polysaccharide Ag + skin protein complexes that are formed
Occurs in 7-10 days

The 2nd encounter has T cells that are sensitized to the Polysaccharide + skin protein complex that are then ready to cause dermatitis
Occurs in 1-2 days (bc it’s T cell mediated)

43
Q

Which autoimmune disease has the clinical manifestations of rashes, arthritis, and glomerulonephritis? What are the most frequent auto-Abs found in this disease?

A

SLE

Anti-DNA Abs (testing for the presence of these anti-nuclear Abs is a diagnostic tool for SLE)

44
Q

What triggers SLE inflammation? Explain why this triggers SLE then give 2 specific examples of this type of trigger.

A

Damage to any tissue can cause previously sequestered self DNA to be released from the damage site.
This provides previously unexposed selfDNA molecules that could potentially activate the self-reactive DNA Abs that cause SLE

  1. Viral infections
  2. UV damage
45
Q

During SLE, state the 2 effects that occur after the formation of the immune complex is formed. What Ig isotype is included inthe immune complex?

A

Fcgamma receptor engagement with a variety of cell types

Complement fixation

(both of these cause apoptosis/tissue damage)

IgG Abs are in the immune complex

46
Q

What disease is characterized by inflammation of the synovium that causes destruction of the joint cartilage and bone? State the 5 cell types that are involved in this type of autoimmune reaction.

A

Rheumatoid Arthritis (RA)

Th1 cells
Th17 cells
Activated B cells
plasma cells
Resident tissue macrophages
47
Q

Briefly describe the mechanism of Multiple Sclerosis (MS) and state the type of hypersensitivity reaction it is considered to be.

A

T and B lymphocytes mediate MS by becoming activated by the self Ags in Myelin in the brain.

T cells become activated secrete IFNgamma to signal for Macrophages to create ROS and give off excess glutamate

B cells become activated and Secrete auto-antibodies that activate the complement to destroy myelin sheaths

MS is a type IV hypersensitivity reaction

48
Q

Briefly describe the mechanism of Multiple Sclerosis (MS) and state the type of hypersensitivity reaction it is considered to be.

A

T and B lymphocytes mediate MS by becoming activated by the self Ags in Myelin in the brain.

T cells become activated secrete IFNgamma to signal for Macrophages to create ROS and give off excess glutamate

B cells become activated and Secrete auto-antibodies that activate the complement to destroy myelin sheaths

MS is a type IV hypersensitivity reaction

49
Q

Explain how the glutamate secreted by Activated T cells is related to the Oligodendrocytes in the CNS in a MS pt.

A

Oligodendrocytes = cells that myelinate Axons

Oligodendrocytes are very susceptible to even low levels of excess glutamate and will undergo apoptosis if exposed to glutamate

50
Q

What type of Hypersensitivity reaction is Type I diabetes considered? What cells does it affect?

A

Type IV (T cell mediated)

It creates auto-reactive Abs that destroy the Beta cells of the pancreas that secrete Insulin
(APC recognizes self-Ag, presents it to a CD4+ T cell to activate it, and the CD4+ T cell activates a B cell to have it create auto-reactive Abs)

51
Q

State 2 foods/drinks that have been shown to increase the levels of autoantibodies present in the blood that destroy the Beta cells of the pancreas in type I diabetes pts.

A

Milk and Etoh

52
Q

What is a disease that is an exaggerated response to what is considered to be normal microflora in the GI tract? what type of hypersensitivity reaction is this?

A

IBD (Inflammatory Bowel Disease)

Type IV

53
Q

What is the most potent activator of the macrophage activity that causes IBD? what cells secrete this macrophage activator?

A

IFNgamma from Th1 cells

54
Q

What does it mean to say the TNF plays a central role in IBD?

A

TNF promotes the survival/apoptosis resistance of the Effector T cells that are causing much of the IBD symptoms

TNF also causes inflammation and destruction of nearly all of the “self tissues” that are damaged during IBD flare ups

55
Q

State the 6 principles of immunotherapy (goals of immunotherapy to treat autoimmune diseases(

A
  1. Regulatory T cell-based therapies (expand/activate T cells)
  2. Anti-Cytokine Therapies (Anti-TNF Ab)
  3. Intravenous IgG (passive immunity of pooled, non-immune IgG)
  4. Depletion of Immune Cells and Abs (Anit-CD20 Ab for B cells)
  5. Anti-inflammatory Agents (Corticosteroids)
  6. Agents that inhibit cell-to-cell interactions and leukocyte migration (anti CD40L)

(“RAIDAA” Mnemonic)

56
Q

What type of hypersensitivity reaction is RA?

A

Type II and Type IV but it is very unclear

Immunology 2019 (22 decks)

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