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Foundations Week 3 > Immune Pathology I: Immunopathology of Hypersensitivity Reactions > Flashcards

Immune Pathology I: Immunopathology of Hypersensitivity Reactions Flashcards

0
Q

Type II hypersensitivity is mediated by _______.

A

Antibody-mediated

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1
Q

Anaphylaxis

A

Sever systemic Type I hypersensitivity response

  • vascular shcock
  • widespread edema
  • acute respiratory distress (bronchiole constriction with air trapping, laryngeal obstruction, pulmonary edema)
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2
Q

Treatment for Anaphylaxis

A

Rapid delivery of epinephrine (EpiPen)

- decreases vasodilation, relaxes bronchial smooth muscle

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4
Q

Mechanisms of injury (Type II Hypersensitivity)

A
  • tissue damage through activation of complement cascade and PHAGOCYTOSIS by immune cells
  • ->transfusion reactions
  • ->autoimmune hemolytic anemia
  • tissue damage through activation of complement cascade and INJURY from inflammatory cells (release of inflammatory mediators)
  • -> Goodpasture syndrome
  • Direct CELL KILLING by cytotoxic cells (NK cells)?
  • Antibody binding to cell impairs normal function
  • -> myasthenia gravis and Graves’ disease
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5
Q

What are transfusion reactions (Type II Hypersensitivity)?

A
  • Antibodies form against and bind to antigens on incompatible blood
  • leads to lysis of RBCs (hemolysis)
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5
Q

What is Goodpasture’s Syndrome? (Anti-GBM disease)

A

Antibodies produced against components of basement membranes

–>target KIDNEY (glomerular basement membranes) and LUNG (alveolar basement membranes)

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6
Q

What is autoimmune hemolytic anemia? (Type II Hypersensitivity)

A
  • patient forms antibodies against antigens on their own RBCs
  • also leads to hemolysis
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7
Q

What are the treatments for Goodpasture’s syndrome?

A
  • immunosuppressive medications
  • plasma exchange (remove offending antibodies); take out a lot of good antibodies as well while doing this, renders them more susceptible to infection
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8
Q

What are the effects of Anti-GBM disease?

A
  • acute kidney injury with blood in urine

- acute pulmonary hemorrhage

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9
Q

Type III Hypersensitivity is mediated by ______

A

Immune complex

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11
Q

What are the steps of Type III Hypersensitivity?

A

– Antibodies bind to antigen in circulation and form complexes (Ab-Ag)
– Complexes lodge in tissue, activate complement
– Recruitment of inflammatory cells and release of
mediators –> tissue injury

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12
Q

Describe Post-Streptococcal Glomerulonephritis (clinical example of Type III Hypersensitivity)

A
  • Occurs 2-4 weeks after skin or throat infections with certain forms of Streptococcus bacteria
  • Acute kidney disease due to glomerular injury
  • Pathogenesis:
    –> Antibodies form against antigens from the strep
    –>Ab-Ag immune complexes lodge in glomerulus
    –>Complement activated
    –>Acute inflammatory response “glomerulitis”
  • Causes glomerular dysfunction
    • Complete resolution in most cases
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13
Q

What are two clinical examples of Type III Hypersensitivity?

A
  • Systemic Lupus Erythematosus (autoimmune disease)

- Post-infectious glomerulonephritis

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13
Q

Type IV Hypersensitivity are ____-mediated

A

Type IV Hypersensitivity are CELL-mediated

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15
Q

What are the steps of Type IV Hypersenstivity?

A

– First mechanism (delayed type):
• Antigen-presenting cell activates CD4+ T-cells
• CD4+ T-cells activate macrophages, PMN’s  tissue
injury
• If antigen persists, may result in formation of granulomas– 2nd mechanism (cytotoxic type):
• Antigen-presenting cell activates CD8+ T-cells
• CD8+ T-cells directly destroy antigen-bearing cells

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16
Q

What are two types of clinical examples for delayed type, type IV hypersensitivity?

A

Contact dermatitis
Granulomatous inflammatory diseases:
–>TB, sarcoidosis

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17
Q

What are the two mechanisms of Type IV Hypersenstivity?

A
  • First mechanism (Delayed type)

- Second Mechanism (cytotoxic type)

17
Q

What are two types of clinical examples for cytotoxic type, type IV hypersensitivity?

A
  • killing of virally infected cells

- T-cell mediated rejection of transplanted organ

18
Q

Describe contact dermatitis and give its gross and microscopic presentaiton

A
  • Skin reaction which developes following exposure to specific antigen
  • ->latex, poison ivy, poison oak, nicke

Gross examination:

  • erythema (redness of skin) 4-6 hours after exposure
  • induration

Mircoscopic:

19
Q

What is immunopathology?

A
  • the process by which the host’s cells/tissues are injured through the host’s immunologic reaction to a stimulus
  • may be incidental to an appropriate immune response (innocent bystander)
  • may be specifically directed to the host’s cells/proteins/tissues (self response)
20
Q

What is the sequence of events from when a macrophage takes up an antigen (general sequence)?

A

Macrophage takes up antigen and presents it to T and B cells:

  • B lymph activated and differentiates to plasma cell which produces antibodies
  • T lymph activated and releases lymphokines
21
Q

There are four classes of hypersensitivity reactions, define each type.

A
  • type I: allergic/anaphylactic type
  • type II: antibody-dependent type
  • type III: immune complex type
  • type IV: cell-mediated type
22
Q

What are the steps in type I hypersensitivity?

A
  • antigen (i.e. pollen) activates a T helper cell to costimulate a B cell to secrete IgE antibodies
  • IgE secreted and IgE bind to mast cell receptors
  • Mast cells degranulate and release mediators (vasoactive amines, lipid mediators, and cytokines)
23
Q

In repeat exposure of type I hypersensitivity, what occurs?

A
  • Mast cells are activated and release mediators (vasoactive amines, lipid mediators, and cytokines)
24
Q

Vasoactive amines and lipid mediators (released by activated mast cells in type 1 hypersensitivity) result in what?

A

immediate hypersensitivity reaction (minutes after repeat exposure to allergen)

25
Q

Cytokines (released by activated mast cells in type 1 hypersensitivity) result in what?

A

late phase reaction (2-24 hrs after repeat exposure to allergen)
see eosinohpils here

26
Q

What are mediators released by mast cells (type 1)?

A
  • HISTAMINE (involved in vasodilation, increased vascular permeability) - act in minutes after exposure
  • neutrophil chemotactic factor (attract neutrophils)
  • enzymes (cause tissue injury)
27
Q

What are the two forms of type 1 hypersensitivity and give examples

A
  • local
  • ->seasonal allergies/rhinitis, urticaria (hives), asthma, insect bite
  • systemic (anaphylaxis)
28
Q

Asthma (local form of type 1 hypersensitivity) shows what changes in histology of lung tissue?

A
  • thickening of smooth muscle (due to repeated constriction of airways)
  • thickening and wrinkling of basement membrane of bronchioles)
  • increased mucus production
29
Q

What steps are involved in type II hypersensitivity (antibody-mediated type)?

A
  • antigen exposure causes antibodies to be released by B cells
  • antibodies attach to antigens on cells and cause direct injury to cell
30
Q

Contrast Type I and Type II hypersensitivity in terms of cells involved

A

Type I: (ALLERGIC)
- involves B cells (plasma cells) that secrete antibodies; T helper cells that activate B cells; mast cells; antibodies (IgE); eosinophils

Type II: (antibody-mediated)
- host cells; macrophages, NK cells; and the complement system

31
Q

Contrast Type I and Type II hypersensitivity in terms of diseases resulting from each

A

Type I:

  • can cause localized immune response, like HAYFEVER or ASTHMA (wrinkles basement membrane in bronchioles, causing constriction); causes muscular hypertrophy in bronchi; excess mucus glands/hyperplasia. causes air trapping in lungs, narrows laryngeal channel.
  • can cause whole body response, like ANAPHYLAXIS (can cause death in minutes due to respiratory difficulties)

Type II:

  • TRANSFUSION REACTIONS, where body lyses blood cells because it is a mismatch to self (recognized as antigen). AUTOIMMUNE HEMOLYTIC ANEMIAS - can also be drug-induced, like from a penicillin reaction causing the body to destroy the body’s RBCs
  • GOODPASTURE DISEASE: body generates antibodies to the basement membrane in the glomeruli and in the alveoli. Causes pulmonary hemorrhage and blood in the urine.
  • MYASTHENIA GRAVIS and GRAVES’ DISEASE
32
Q

What are the cell/tissue targets for two examples of Type II hypersensitivity?

A
  • Goodpasture disease targets the CELLS IN THE BASEMENT MEMBRANES in the glomeruli and the alveoli
  • hemolytic anemia can be caused by a drug-induced reaction to self RBCs; or in a mismatched transfusion, the body will attack RBCs
33
Q

What is Type III hypersensitivity (definition)?

A

Antigen-antibody complexes circulate in the bloodstream and deposit in tissues, leading to localized inflammation and tissue damage

34
Q

What is Type II hypersensitivity (definition)?

A

Antibodies directed toward antigens present on cells or other tissue components, causing cell/tissue damage

(when ag-ab complexes activate complement pathway, various complement components are consumed and level of complement in blood will fall - useful in diagnosis)

35
Q

What is Type I hypersensitivity (definition)?

A

Rapidly evolving immune reaction occurring within minutes of combination of antigen and antibody bound to previously sensitized cell

36
Q

What is Type IV hypersensitivity (definition)?

A

Cell-mediated tissue damage caused by sensitized T-lymphocytes

37
Q

Contrast Types I and III hypersensitivities

A

Type III:
small Ag-Ab complexes float through circulatory system. Due to size, they are less likely to be broken down in liver or spleen. Eventually they get stuck somewhere in circulation. They activate complement, which attracts neutrophils, which can then release proteolytic enzymes. Type III mostly mediated by IgG and some IgM antibodies. The antigens then are more likely to cause these classes of antibodies to be released, and these types of antibodies cannot cause type I hypersenstiivity.

Type I:
involves antigens and antibodies that are recognized by mast cells. These particular antigens are more likely to produce a response in the form of IgE antibody, which then interacts with mast cells which release histamine. Individuals more prone to Type I hypersensitivity preferentially produce more T helper cells that favor IgE class switching.

Mechanism in each is fairly similar, but different responses due to Ig class.

38
Q

Outline the immunologic steps in the development of post-Streptococcal glomerulonephritis as an example of type III hypersensitivity.

A
  • post-streptococcal glomerulonephritis occurs after an acute infection with Streptococcus
  • as infection occurs, body recognizes pathogen as foreign and will mount an immune response to fight it off. Antibody will form.
  • takes about 2-4 weeks for antibody levels to rise enough to cause this problem
  • antigen-antibody complexes (with pathogen) can become lodged in glomerulus
  • blood can’t flow through the glomerulus; pressure builds, and the glomerulus can become damaged
  • causes glomerular injury; acute renal disease
  • usually completely resolves
39
Q

What are three other diseases (other than post-Streptococcal glomerulonephritis) mediated by Type III hypersensitivity?

A
  • serum thickness (rare now), due to treatment with serum from animal source. this would provide antibodies but also proteins from the animal that the body recognizes as antigenic. 10-14 days later blood would develop in urine due to glomerular damage
  • systemic lupus erythematosus
  • polyarteritis
40
Q

Contrast the elements of Type III (immune complex type) from those of Type IV (cell-mediated) delayed hypersenstivity

A

Type IV delayed

  • activated CD4 T cells release cytokines that either
  • -> activate macrophages
  • -> call in neutrophils that will cause tissue injury
  • activated CD8 T cells directly lyse cells
  • the reaction is delayed (due to pathway of B and T cells)

Type III
- Ag-Ab complexes free float through circulation and get stuck in areas where they impair the function, like in the glomeruli. This raises pressure and causes glomerular damage.

Type IV uses CD4 and CD8 cells to activate cell lysis or other WBCs.
Type III uses Ag-Ab complexes, of which the antibodies were secreted by B cells

41
Q

List the series of cellular/tissue events which lead to the formation of a granuloma

A
  • antigen-presenting cell engulfs a pathogen and presents it on MHC II to a CD4+ T helper cell
  • the T-helper cell releases cytokines that signal monocytes to travel into the tissues
  • monocytes differentiate (with the help of cytokines)
  • -> into macrophages, which phagocytose foreign material, and combine to form giant cells
  • -> into epithelioid cells, which are large and secrete many things into the granuloma
  • lymphocytes enter the area around the edge of the granuloma; they are memory cells in case the antigen “flares up” and more immune response is needed
  • fibroblasts are also located around the granuloma to lay down collagen as needed. Old granulomas may have very few cells and be made mostly of collagen

Foundations Week 3 (12 decks)

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