Type 4 Hpersensitivity Rxns Flashcards

1
Q

Type w Hypersensitivity reactions are mediated by _______ and utilize _________ antigens

A

T Cells

Soluble and Insolube

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2
Q

Type of Hypersensitivity in Type 4?

A

Most are delayed type hypersensitivity

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3
Q

Th1 Type IV reaction.

Name the antigen type, effector mechanism

A

Soluble antigen

Macrophage Activation

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4
Q

Th2 Type IV reaction.

Name the antigen type, effector mechanism

A

Soluble Antigen

Eosinophil Activation

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5
Q

CTL Type IV reaction.

Name the antigen type, effector mechanism

A

Cell Associated Antigen

Cytotoxicity

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6
Q

Example of TH1 cell type four hypersensitivity reactions

A

Contact Dermatitis

Tuberculin Rxn

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7
Q

Example of TH2 cell type four hypersensitivity reactions

A

Chronic Ashtma

Chronic Allergic Rhinitis

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8
Q

Example of CTL cell type four hypersensitivity reactions

A

Contact Dermatitis

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9
Q

Example of a Type 4 allergy response

A

Poison Ivy

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10
Q

Example of a Type 4 Transplantation Rxn

A

Acute Rejection

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11
Q

Example of Type 4 mediated autoimmunity

A

Type I Diabetes

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12
Q

Difference between delayed type hypersensitivity and contct hypersensitivity exposure.

A

DTH – Proteins Injected into Skin

Contact – Small, Absorbed into Skin

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13
Q

Examples of antigens in Type 4 DTH?

A

Insect Venom

TB Test

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14
Q

Consequences of delayed type hypersensitivity rxn?

A

Local Skin Swelling (erythema, induration, cellular infiltrate, dermatitis)

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15
Q

Examples of antigens of Contact hypersentivity

A

Pentadecacatechol
DNFB
Small Metal Ions (Nickel, Chromate)

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16
Q

Consequences of a Type 4 contact hypersensitivity reaction

A

Local epidermal reaction

Erythema, Cellular Infiltrate, Vesicles, Intraepidermal Abscess

17
Q

What happens in gluten-sensitive enteropathy

A

Gliadin in the GI tract triggers villous atrophy in small bowel, malabsorption

18
Q

Four types of Type 4 reactions

A

Contact hypersensitivity
Tuberculin
NK and T-cytotoxicity
Granulomatous

19
Q

Cytokines involved in Type 4?

A

IFN-g, TNF-a, IL-3, IL-12, GM-CSF

20
Q

Diseases associated with granulomatous hypersensitivity? (6)

A
Leprosy
Tuberculosis
Schistosomisis
Sarcoidosis
Crohn's
Hypersensitivity pneumonitis
21
Q

Ways a DTH reaction can be assessed?

A

Patch Test

Skin Test to Evaluate CMI

22
Q

What is pentadecacatechol?

A

The causative agent of contact sensitivity in poison ivy

23
Q

How does Type 4 rxn sensitivity first encounter play out?

A
Penetration into skin
Modification of self protein
Capture by antigen presenting cells
presentation in LN
Activate native T cells
Generation of poison ivy specific T cells
24
Q

Final result of first poison ivy exposure?

A

Asymptomatic

25
Q

How does Type 4 rxn sensitivity play out in 2nd chance

A

Penetration into skin
modification of self proteins
Captured by APCs, presented in LN
Memory T Activation

26
Q

Final result of second poison ivy exposure?

A

Activation of downstream effector cells

Phagocyte recruitment and Inflammation

27
Q

Where are Langerhan’s Cells located?

A

Epidermis

28
Q

Lymphocytes found in skin must express…

A

Curaneous Lymphocyte Antigen (CLA)
P-/E- Selectin Ligands
Chemokine Receptors (CR4, CCR8, CCR10)

29
Q

Describe the steps of a skin DTH rxn

A

Contact sensitizing agent penetrated skin
Taken up by Langerhan’s
Lang. present self peptides haptenated with the contact sensitizing agent to TH1 (releasing more IFNg)
Activated kera. secrete IL1, TNFa, IL-8, IL-9, and MIG
TH1 activation of macrophages to secrete mediators of inflamm

30
Q

Four downstream effectors secreted by Th1 cells

A

Chemokines
IFNg
TNFa and LT
IL3/GM-CSF

31
Q

What to TH1 chemokines do?

A

Recruit Macrophages

32
Q

What to TH1 IFNg do?

A

Activate macrophages, increasing release of inflamm mediators

33
Q

What do TNFa and LT do?

A

Increase expression of adhesion molecules on B vessels

Local Tissue Destruction

34
Q

What does IL-3/CM-CSF do?

A

Monocyte production by bone marrow cells

35
Q

How is contact hypersensitivity treated?

A

Corticosteroids

36
Q

What do corticosteroids do?

A

Suppres Inflammatory genes

Induce synthesis of anti-inflammatory proteins