Type III and IV hypersensitivity

Question 1

what happens if immune complexes are not cleared effectively?

Answer 1

may be deposited in tissues or in blood vessels and cause:
- Vasculitis if in bloodvessel
- Glomerulonephritis if in kidney
- Arthritis if in joints

Question 2

CM of Type III hyper

Answer 2

1) fever,
2) rashes,
3) joint pain,
4) lymph node enlargement, and
5) protein in the urine

Question 3

Type III hypersensitivity reactions May trigger release of inflammatory mediators and vasoactive mediators such as?

Answer 3

Histamins, Proteases (Tryptase)

Question 4

Examples of Type III hyper. disorders

Answer 4

1) SLE
2) Arthus rxn
3) Serum sickness

Question 5

Clinical featues of SLE

Answer 5

1) Butterfly facial rash
2) Arthritis
3) vasculitis
4) Nephritis

Question 6

Which type III hypersensitivty rxn presents w/ Local pain and edema and is associated w/ intradermal injection of Ag into a presensitised (circulating IgG) individual?

Answer 6

Arthus reaction

Question 7

Antigens invlovled in SLE?

Answer 7

dsDNA, Smith , (other nucleoproteins)

Question 8

A localized type III hypersensitivity rxn ?

Answer 8

Arthus reaction

Question 9

————- : An inflammatory reaction induced by injection of an antigen in the skin of a sensitized individual with high levels of circulating antibody (IgG) against the sensitized agent with high levels of circulating antibody against the sensitizing agent

Answer 9

Arthus reaction

Question 10

An inflammatory Arthus reaction is inititated within ——- hr post injection

Answer 10

4-10 hrs

Question 11

CM of Arthus reaction

Answer 11

1) Odema
2) Localized bleeding at injection site
3) Fibrinoid necrosis

Question 12

Example of a transient (short-lived) immune-complex mediated syndrome

* Type III hyper.

Answer 12

Serum sickness

Question 13

Explain what causes Serum sickness and how the immune complexes are cleared

Answer 13

A systemic type III hyper induced by injection of serum w/ foreign proteins (species) –> development of Abs against forgein Proteins –> antibody-antigen complexs form and deposit in tissues –> complement activation -> inflammation and tissue damage

* serum examples –> theraputic horse anti-serum against snake venoms

Question 14

Antigens invloved in serum sickness + CM

Answer 14

Ags: Various proteins
CM : Arthritis, vasculitis, nephritis (chills, fever and rash)

Question 15

The antibodies involved in type III reactions are of ——– class

Answer 15

IgG

Question 16

Type IV hyper. is mediated by?

Answer 16

antigen-specific effector Tcells
Aka Delayed type hype, (DTH)

Question 17

**

DTH reactions are elicited by?

Answer 17

CD4+ TH1, TH17 or CD8+ CTLs
–> activate macrophages, recruit neutrophils and induce inflammation

Question 18

**

Most common type IV hyper?

Answer 18

Contact dermatitis
(after exposure to Toxicodendron species e.g., poison ivy, poison oak, poison sumac)

• she might ask they type of toxins that causes this (not sure)

Question 19

How can DTH responses be avoided?

Answer 19

avoid the causative agent

• dont think we need to know Tx in general so info

Question 20

When is DTH initiated?

Answer 20

it is a delyaed reaction that developes in a sensitized individual in 24-72hrs

Question 21

which 2 pahses are involved in Type IV hyper.?

Answer 21

1) Sensitization phase (initation of DTH)
2) Effector phase (second exposure to sensitized ag)

Question 22

Exaplin the Sensitization/ Effector phase of DTH

Answer 22

1) Sensitization phase:
initial exposure to Ag triggers the production of CD4+ TH1 subset (but can also include TH17, CD8+T)

2) Effector phase:
Second exposure to sensitized antigens –> Induces the production of inflammatory Cytokines by Effector CD4+ Th1 cells –> These recruit and help activate macrophages in TH1 –mediated responses (cytokines such as IFNγ)

Question 23

The principal effector cells of the DTH response are ————- , which exhibit enhanced phagocytosis and an increased ability to kill microorganisms

Answer 23

Activated macrophages

Question 24

When does the effector phase in DTH becomes activated?

Answer 24

Following the initial sensitization, a period of 1–2 weeks is required for antigen-specific T cells to be activated, clonally expand and mature into effector cells

Question 25

A prolonged DTH response can lead to formation of ————

Answer 25

Garnuloma
(e.g. TB)

Question 26

Test to detect DTH reactions

Answer 26

Skin Test
* Injection of a small amount of antigen under the skin

Question 27

what is a positive DHT skin test ?

Answer 27

Development of a red, slightly swollen, firm lesion 48-72 hrs after injection of ag under the skin
- this indicates the presence of Sensitized TH1 or TH17 cells against the Antigen

* test commonly used for TB exposure

Question 28

Examples of Type IV hypersensitivities

Answer 28

1) Multiple sclerosis
2) Rheumatoid arthritis
3) Type I diabetes
4) Celiac disease

* look at the table p.13 in Type IV lecture

Question 29

pathogenesis of celiac disease

Answer 29

this is mediated by an immune response to Gliadin
1) Inflammation of the small intestine (villus atrophy) is caused by CD4+ T cells responding to gliadin that is deamidated by tissue transglutaminase (tTG) and presented by HLA-DQ2 class MHC II allele

* know That Gliliadin s involved w/o patho/bio part (HLA bla bla)

Question 30

All patients w/ celiac disease have serum ————— against tTG (autoantibodies) that constitutes a sensitive and specific test

Answer 30

serum IgA

Question 31

**

Celiac disease is mediated by an immune response to?

Answer 31

Gliadin

Question 32

**

CF of celiac disease

Answer 32

Gluten-sensitive enteropathy
(bloating, nausea etc)

Question 33

A DHT skin test against TB?

Answer 33

tuberculin test ( individuals are injected intradermally with tuberculin)

note:
* Individuals who have been exposed to the bacterium, either by infection or by immunization with the BCG vaccine –> develop a localized T-cell mediated inflammatory response which evolves over 24-72hours
* The response is caused by TH1 cells
* which enter the site of antigen injection, recognize complexes of peptide:MHCclass II on antigen-presenting cells and release inflammatory cytokines such asIFN-γ