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Immunology > Week 7: Hypersensitivity > Flashcards

Week 7: Hypersensitivity Flashcards

1
Q

What causes Type 3 pathology?

A

Formation of immune complexes and resulting inflammation

Subacute

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2
Q

What components of Type 3 HS?

A
  1. Antigen
  2. Antibody
  3. Complement
  4. Innate immune cells
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3
Q

How do you form an immune complex?

A
  1. Antibodies bind to a soluble antigen
  2. Forms a lattice like structure
  3. Fc portion of the antibody can bind to C1q and 3b or Fc receptors on phagocytic cells
  4. C3b is recognized by CR1on RBC, transports the IC to the spleen and liver where they are phagocytized by resident macrophages
  5. RBCs are returned to circulation
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4
Q

What happens if immune complexes aren’t cleared effectively?

A

They may deposit in tissues and cause an inflammatory response

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5
Q

What are the phases of type 3 HS disease?

A
  1. Antigen-antibody complex formation in circulation and localized area
  2. Deposition of immune complexes in vasculature or tissues
  3. Injury of issues by inflammatory response
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6
Q

What are the categories of ICs?

A
  1. Small
  2. Medium
  3. LArge
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7
Q

What are large ICs?

A
  1. Don’t trigger an immune response
  2. Can be cleared by RBCs
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8
Q

What are medium IC?

A
  1. Deposits in vessel walls or in tissues
  2. Triggers an immune response
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9
Q

What are large IC?

A
  1. Able to fix complement
  2. Cleared by phagocytes
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10
Q

What occurs in the phase 2 response in type 3 HS?

A
  1. IC form and deposit on the basement membrane of the blood vessels
  2. Triggers an inflammatory response mediated by complement activation
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11
Q

What is activated in the phase 3 response in type 3 HS?

A
  1. C1q binds to IgG or IgM and initiates complement cascade
  2. C3b deposits on the immune complex
  3. C5a (anaphykatoxins) attracts neutrophils to the site of IC deposition
  4. Neutraphils degranulate
  5. enzymes and ROS are released that cause tissue damage and necrosis
  6. Fc portions of Ab within IC’s can bind to mast cells, neutrophils and macrophages Fc receptors.
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12
Q

What is the phase 3 type 3 response?

A

Trigger inflammatory mediators and vasoactive mediators such as:
1. Proteases released may damage connective tissues
2. Clots may form as complexes activate platelets

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13
Q

What are symptoms of phase 3 response of type 3 HS?

A
  1. Fever, rash, joint pain, lymph node enlargement, proteinurina
  2. Vasculitis if in blood vessels
  3. Glomerulonephritis if in kidney
  4. Arthritis in joints
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14
Q

How are immune complex mediated HS?

A

Response spontaneously but are cleared so long as antigen eventually goes away

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15
Q

What are autoantigens?

A

Involved in immune complex-mediated reactions
1. Self antigen cannot completely go away in such a case
2. Seen in autoimmune diseases

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16
Q

What are the types of type 3 responses?

A
  1. Localized
  2. Systemic
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17
Q

What are localized responses?

A

Antigen can be:
1. Injected vaccinations
2. Inhaled (farmer’s lungs)
3. Ingested (gluten)

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18
Q

What are systemic responses?

A
  1. Serum sickness (exogenous serum)
  2. Raynaud phenomenon (cyroglobins)
  3. Systemic lupus erythematosus (endogenous antigen)
  4. Rheumatoid arthritis (endogenous antigen)
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19
Q

What is an arthus?

A

A local HS reaction that can be triggered in the skin of sensitized individuals that have preformed circulating antibodies (IgG) against the antigen

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20
Q

What is the physical reaction of arthus?

A
  1. Inflammation and swelling early and can be hemorrhagic and necrotic
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21
Q

What would arthus peak?

A
  1. 4-10hrs post injection
  2. May take place following a booster immunization
  3. May take place after a rapid, localized type 1 reaction to an insect bite
  4. May develop in lungs after inhalation of antigen
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22
Q

What is serum sickness?

A

Systemic IC and complement dependent inflammatory reaction to an extrinsic antigen

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23
Q

What makes serum sickness severe?

A

Dose dependent

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24
Q

What is the 1st exposure of serum sickness?

A

Antigen without preexisting antibodies is approximately 1-2 weeks

25
Q

What is the 2nd exposure of serum sickness?

A

Sensitizing antigen is such faster and stronger (2-36hr)

26
Q

What can serum sickness inflammation lead to?

A

Vasculitis in the vessels glomerulonephritis in the kidney, arthritis in the joint

27
Q

What are the common manifestations of serum sickness?

A
  1. Blotchy skin rashes
  2. Joint pain
  3. Peripheral edema
  4. Fever
28
Q

What is the immune response to serum sickness?

A
  1. B cells take up antigen, present to T helper cells which differentiate to plasma cells
  2. Plasma cells form antibodies against foreign antigen
  3. Antibodies form ICs with antigen that deposit in the basement membrane of the vessels
  4. ICs activate complement
  5. Draws in neutrophils that degranulate and cause tissue damage
  6. Macrophages release pro-inflammatory cytokines
  7. Mast cells release histamines
29
Q

What could happen if you inject an individual with mouse monoclonal antibody?

A

Immune response that results in antibodies formed against that antigen forming ICs that lead to inflammatory response

30
Q

What are the symptoms of response to serum sickness?

A
  1. Fever
  2. Vasculitis (vessels due to IC deposition and inflammatory response)
  3. Arthritis (Joint)
  4. Nephritis (Kidney)
31
Q

What is the treatment for type 3?

A
  1. Drugs are used to treat the symptoms of the reaction
  2. Non steroidal anti inflammatory drugs
  3. Antihistamine
  4. Corticosteroids
32
Q

Describe the incidence of serum sickness?

A

Decreasing due to reduction of admin of foreign antigens

33
Q

When is incidence higher of serum sickness?

A

Use of anti-venom and rabies serum treatments

34
Q

What are common causes of serum sickness?

A
  1. ANntitoxins
  2. Antivenins
  3. Hormone from other species
  4. Streptokinase
  5. Vaccines
35
Q

What types of monoclonal antibodies that cause serum sickness?

A
  1. Infliximab
  2. Omalizumab
  3. Rituximab
36
Q

What types of insect bites/stings that cause serum sickness?

A
  1. Bees
  2. Wasp
  3. Mosquitos
  4. Ticks
37
Q

What is type 4 pathology?

A
  1. Purely cell-mediated rather than Ab mediated
  2. Initiated by T cells
  3. Requires a delay for the reaction to develop
  4. Characterized by recruitment of macrophages at inflammation site
38
Q

What can cause type 4?

A

Poison ivy (dermatitis)

39
Q

What is delayed-type HS?

A
  1. Initiation of DTH involves sensitization by antigen
  2. Antigen is transported from area of contact to lymph nodes to active naive T cells
  3. Antigen is presented by MHC 2 molecules to AS T cells (langerhans)
  4. APC cells secrete IL12 (polarizing cytokines for TH1 cells)
40
Q

What is DTH response mediated by?

A
  1. Primarily mediated by TH1 effector T cells
  2. Response takes 1-2 weeks of time
  3. During this time T cells: become activated, clonal expand, mature into effector T cells
41
Q

What is DTH effector phase induced by?

A
  1. Second exposure to a sensitizing antigen
  2. Stimulates previously activated TH1 cells to secrete inflammatory cytokines
  3. Cytokines recruit and help activate macrophages and other inflammatory cells
  4. DTH secondary response to the second contact with the antigen is around 24-48hr
42
Q

What is exhibited when activated macrophages in DTH?

A
  1. Enhanced phagocytosis
  2. Produce more cytokines and chemokines to draw more neutrophils and monocytes to area
  3. Enhanced ability to remove extracellular antigens
43
Q

What is TH1 initiate response allude?

A
  1. Chemikines induce an influx of macrophages
  2. TNF and IFN-y induce blood monocytes to migrate to area of antigen exposure and differentiate into macrophages
44
Q

What is the DTH response to intracellular infection?

A
  1. Enzymes produced from macrophages cause the nonspecific death of cells in area killing intracellular pathogens
  2. TB hides in the macrophages endosome and prevents it from joining with lysosome
  3. IFN-y secreted by TH1 T cells allows the macrophage to overcome this block and kill bacteria
45
Q

What is DTH response on antigens that are harder to clear?

A
  1. Prolonged DTH becomes destructive to tissues
  2. Causes the formation of destructive multinucleate giant cell and granulomas
46
Q

What are multinucleate giant cells?

A

Formed from macrophages that fuse together and form nodules

47
Q

What are granulomas?

A
  1. Develop when there is continuous activation of macrophages and adhere to each other
48
Q

What is granulomatous response?

A

Granulomas that release large amounts of lytic enzymes that damage blood vessels and lead to tissue necrosis

49
Q

What occurs during M TB infection?

A
  1. TH1 cells activate macrophages
  2. Macrophages release enzymes to kill infected cells
  3. If macrophage can’t clear the infection, the DTH persists
  4. Activated macrophage wall off the bacteria in the lung to contain it in the granuloma
  5. Lytic enzymes from the macrophages within the granuloma damages the lung tissue
50
Q

How can we use skin tests to detect DTH?

A
  1. Injecting a small amount of Ag under the skin
  2. PPD antigen is taken up by local macrophages and DCs and is loaded into MHC II
  3. Antigen is presented to anti-TB TH1 cells
  4. TH1 cells produce inflammatory cytokines to activate macrophages and attract more macrophages
51
Q

What is the antigen used for DTH?

A

Purified protein derivative (PPD) of the cell wall of M TB

52
Q

What is TB detection on a skin test?

A
  1. If a red, slightly swollen, firm lesion develops in 48–72 hours, the test is positive.
53
Q

What can a skin test not determine with TB?

A

Can’t determine if it is an active infection is occurring or if the individual already overcame an infection

54
Q

How is contact dermatitis a type 4 HS?

A

Sensitization can occur when a reactive chemical compound (irritant) binds to skin proteins-haptens

55
Q

What are happens?

A

Small, non-immunogenic molecules that are usually nonbioloigic in origin that behave like synthetic epitopes

56
Q

When are happens reactive?

A
  1. They bind to protein that cause them to become immunogenic
  2. Could be induced by cosmetics, pharmaceuticals, industrial chemicals, hair dyes, metal ions
  3. Modified proteins are then presented to T cells
  4. Can cause strong cell-mediated responses against skin cells, inducing blisterlike lesions and rashes
57
Q

What is urushiol?

A
  1. Poison ivy can penetrate intact skin and bind to proteins on cells
  2. It is taken up by DCs in the skin and presented by MHC class II molecules
  3. DC travels to the draining LN when it presents the antigen to T cells that develop into TH1 cells
  4. By the time there is enough T cells to mount a response, the antigen has been washed away from the skin
  5. No reaction occurs but you become sensitized
58
Q

How can urushiol cause contact dermatitis?

A
  1. Urushiol is taken up and presented on MHC class II on DCs.
  2. This antigen is presented to anti-urushiol T memory cells and they become activated and rapidly expand.
  3. TH1 cells secrete IFN-g to attract large numbers of macrophages.
  4. This produces an inflammatory response in approximately 6-12 hours following exposure.
  5. Macrophages release inflammatory cytokines, lytic enzymes, and ROS species causing tissue damage
  6. Breakdown of the skin leads to blistering.
  7. Sensitized TH1 cells respond through MHC II interaction with APC and secrete IFN-g
  8. CTLs can recognize hapten presented by MHC class I molecules on epithelial cells and cause cytotoxic killing of the affected cell.
  9. Haptens are small molecule antigens that are recognized by a TCR.
    10 .Macrophages are activated by IFN-g and secrete cytokines and lytic enzymes
59
Q

When would all HS responses occur?

A

2nd exposure to antigen

Immunology (17 decks)

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