15 Hypersensitivity Flashcards

1
Q

What is Hypersensitivity?

A

Exaggerated immune response that causes damage to the individual

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2
Q

What is immediate hypersensitivity?

A

an exaggerated immune response mediated by an antibody or antigen-antibody complexes that manifests within minutes - hours after exposure to an antigen

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3
Q

What is the Type I immediate hypersensitivity?

A

IgE-mediated hypersensitivity

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4
Q

What is the Type II immediate hypersensitivity?

A

IgG or IgM-mediated hypersensitivity

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5
Q

What is the Type III immediate hypersensitivity?

A

Immune complex-mediated hypersensitivity

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6
Q

What is delayed-type hypersensitivity (DTH)?

A

a type-sensitive response that is mediated by T helper cells that release various cytokines/chemokines

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7
Q

When does DTH response take place?

A

generally 2-3 days after T helper cells interact with an antigen

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8
Q

What is the Type IV DTH hypersensitivity?

A

cell-mediated hypersensitivity (T cells)

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9
Q

What are the four types of hypersensitivity reactions?

A

Type I: Allergy and Atopy
Type II: Antibody-mediated hypersensitivity
Type III: Immune complex-mediated hypersensitivity
Type IV: Delayed-type hypersensitivity

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10
Q

What is an allergy?

A

An allergy is a type I hypersensitivity reaction

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11
Q

What is responsible for type I hypersensitivity?

A

IgE antibodies interact with a multivalent antigen, so, IgE antibodies

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12
Q

How do allergies come to be?

A

IgE antibodies cross-link Fcε receptors on the surfaces of innate immune cells, and granule contents are released, like histamine, heparin, proteases, leukotrienes, prostaglandins, and chemokines. Mediators act up on surrounding tissues and cells which causes the symptoms of allergies. (Note: Abs are not harmful by themselves, it’s the linking of the Fcε receptors via IgE antibodies which is why they are the cause of allergies)

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13
Q

What are allergens?

A

Specific type of antigen that induces a type I hypersensitivity reaction. Examples: nuts, milk, dust mites, penicillin, birch trees

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14
Q

Atopy

A

Abnormality in people that causes a predisposition to generate IgE Abs against common environmental antigens. Normally, IgE response is against parasitic infection.

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15
Q

Where are mast cells located?

A

Tissue

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16
Q

Where are basophils located?

A

They are in circulation throughout the immune system and are recruited into inflammatory sites

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17
Q

What helps Abs when fighting against immune reactions?

A

Granule contents (histamine, heparin, proteases) and mediators around the affected tissues/cells that cause symptoms

18
Q

What is the high-affinity IgE receptor? What does it do?

A

FcERI, responsible for most allergy symptoms; found on basophil/mast cells

19
Q

What is the low-affinity IgE receptor? What does it do?

A

FcERII, regulates production of IgE by B cells

20
Q

True or False: Innate immune cells produce molecules responsible for Type I hypersensitivity symptoms

A

TRUE.

21
Q

What are the steps of response from Type I hypersensitivities?

A

Early response: within minutes of allergen exposure, mediated by mast cell granule contents

Late response: hours later from recruited inflammatory cell types (ex. neutrophils)

Third phase: 3rd day after exposure, peaks at 4th day post-exposure. Massive eosinophil infiltration

22
Q

What is systemic anaphylaxis? What is it caused by? What cures it?

A

Shock-like, often fatal state with a within-minutes onset. Caused by venom (bee, ants), drugs (insulin, penicillin), or food (seafood, nuts). Cure: epinephrine

23
Q

What is anaphylaxis?

A

Serious allergic reaction with rapid onset that may cause death

24
Q

What are some examples of localized hypersensitivity reactions (atopy scenarios)?

A

Hay fever, asthma, eczema, and food allergies

25
Q

True or False: Type I hypersensitivity is environmental-only, not genetics-based

A

FALSE: allergy-linked genes include proteins (MHC, cytokines/chemokines), Airway remodeling genes, and transcription factors that regulate epigenetic modifications

26
Q

What can be done about allergies?

A

Hyposensitization (repeated low-dose exposures), dosing of antihistamines/ihalation corticosteroids, exposure to pathogens early in life to increase T-cell balance

27
Q

What is an example of Type II hypersensitivity?

A

Transfusion reactions

28
Q

Is IgG or IgM-mediated hypersensitivity a type I or type II reaction?

A

Type II

29
Q

What are Blood group Ag?

A

Carbohydrates

30
Q

True or False: Adults possess antibodies to the blood type they do NOT have

A

TRUE! This is why if a transfusion of a diff. blood type is given, the antibodies will attach to the donor blood cells to degrade them, which can build to toxic levels of degraded RBC components

31
Q

What is an example of a disease caused by Type II reactions?

A

Hemolytic disease in newbornes

32
Q

What is another name for Type III hypersensitivity?

A

Immune complex-mediated hypersensitivity

33
Q

How can immune complexes damage tissues?

A
  • May trigger release of inflammatory/vasoactive mediators which recruit neutrophils
  • symptoms that follow include fever/rashes/protein in the urine
  • if the Ags don’t go away, complexes aren’t cleared, like in autoimmune complexes
34
Q

What are some examples of Type III hypersensitivity reactions?

A

Multiple sclerosis, autoimmune diseases, and malaria

35
Q

What is another name for Type IV hypersensitivity?

A

Delayed type hypersensitivity

36
Q

True or false: DTH is Ab mediated

A

FALSE: DTH is purely cell-mediated and initiated by t cells

37
Q

What is required from Type IV hypersensitivity? What characterizes it?

A

Delayed-type hypersensitivity (DTH) requires a delay for the reaction to develop. Characterized by macrophage recruitment at the inflammation site

38
Q

What is the most common example of DTH?

A

Poison ivy contact dermatitis

39
Q

What does the initiation of a type IV DTH response involve?

A

Sensitization by an antigen, or the sensitization phase. Initial exposure triggers T-cell response production (Often CD4+TH1), takes 1-2 weeks to settle in

40
Q

What does the second exposure to a sensitizing Ag for DTH do?

A

Induces production of TH1 inflammatory cytokines that help recruit/activate macrophages, leading to granuloma formation. AKA the effector phase

41
Q

How can a DTH reaction be detected? When is this used commonly?

A

Skin test: inject small amount of Ag under skin and wait to see if a red, firm lesion develops in 48-72 hrs for a positive result. Commonly used in the US for tuberculosis (TB) exposure

42
Q

What antibodies/lymphocytes are induced by which reactions?

A

I - IgE
II - IgM, IgG
III - IgG
IV - TH1 cells