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Immunology - Unit 4 - Zach H. > Hypersensitivity Disorders > Flashcards

Hypersensitivity Disorders Flashcards

1
Q

What is a hypersensitivity reaction?

A

Immune responses that cause tissue injury are called hypersensitivity reactions.

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2
Q

What are hypersensitivity diseases also known as?

A

immune-mediated inflammatory diseases

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3
Q

What are some things that may cause hypersensitivity reactions to arise?

A
  • Uncontrolled or abnormal responses to foreign Ags.

- Autoimmune responses against self Ags.

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4
Q

How are hypersensitivity reactions classified?

A

According to the mechanisms of tissue injury.

> Type I hypersensitivity (immediate)
Type II hypersensitivity
Type III hypersensitivity
Type IV hypersensitivity (delayed)

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5
Q

What causes type I hypersensitivity?

A

Mediated by IgE and results from the actions of mediators secreted by the mast cells.

This reaction is most often triggered by ENVIRONMENTAL Ags which activate mast cells in an IgE-dependent manner.

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6
Q

What causes type II hypersensitivity?

A

Mediated by Abs that bind tissue Ags and cause complement-dependent tissue injury and disease.

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7
Q

What causes type III hypersensitivity?

A

Mediated by Abs that bind to circulating Ags to form immune complexes, which deposit in vessels and cause complement-dependent injury in the vessel wall (vasculitis).

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8
Q

What causes type IV hypersensitivity?

A

Mediated by T cells diseases and results from inflammation caused by cytokines produced by CD4 Th1 and Th17 cells, or killing of host cells by CD8 CTLs.

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9
Q

What does ATOPY mean?

A

Refers to the genetic tendency to develop allergic diseases.

Individuals with a strong propensity to develop allergic reactions are said to be atopic.

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10
Q

In type I hypersensitivity, what is the sequence of events in the development of immediate hypersensitivity?

A

(1) PRODUCTION of IgE after activation of Th2 cells by primary exposure to allergens.
(2) BINDING of the IgE to Fc receptors of mast cells.
(3) RELEASE of mediators by mast cell after secondary exposure to the Ag and cross-linking of the membrane-bound IgE by Ags.

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11
Q

Immediate vascular and smooth muscle reaction to allergen develops within minutes after a challenge. What is the morphology of the immediate reaction characterized by?

A
  • vasodilation
  • congestion
  • edema
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12
Q

How long after the initial challenge does the late-phase reaction develop?

A

2-24 hours later

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13
Q

What is the late-phase reaction in type I hypersensitivity characterized by?

A

An inflammatory infiltrate rich in eosinophils, neutrophils, and T cells.

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14
Q

Mast cell mediators are responsible for acute reactions and inflammation, the hallmarks of immediate hypersensitivity. What are the most important mediators?

A
  • VASOACITVE AMINES
  • *histamine is the major amine that causes the dilation of small blood vessels and increases vascular permeability.
  • PROTEASES
  • *cause damage to local tissue.
  • PROSTAGLANDINS (PGs)
  • *cause vascular dilation.
  • LEUKOTRIENES (LTs)
  • *stimulate prolonged smooth muscle contraction.
  • CYTOKINES
  • *induce local inflammation (the late-phase reaction).
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15
Q

In type I hypersensitivity reactions, what is the mechanism of an initial allergen encounter?

A

> Contact with allergen: inhaled, ingested, injected or by contact.

> Adaptive immune response by B cells that mature into plasma cells to make IgE to allergen.

> IgE enters circulation and is rapidly bound by FcRe (CD23) on mast cells in the tissues.

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16
Q

In type I hypersensitivity reactions, what happens in a subsequent allergen encounter?

A

> Cross-linking causes mast cell degranulation that releases:

 - vasactive amines (histamine)
 - cytokines/chemokines 
 - lipids

thus, vascular smooth muscle contraction, endothelial vasodilation, and leukocyte chemotaxis and activation

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17
Q

What is asthma?

A

Asthma is a reversible airway obstruction often caused by the release of inflammatory mediators from mast cells upon encounter with an allergen.

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18
Q

How do the inflammatory mediators from mast cells upon encounter with an allergen cause airway obstruction?

A

Inflammatory mediators cause the loosening of tight junctions in the bronchiole epithelium, increased capillary permeability, and spasmatic contraction of smooth muscle surrounding the bronchi.

This temporarily decreases the size of the bronchial lumen, resulting in shortness of breath.

Bronchospasms triggered by non-immunologic stimuli such as cold, viral infections, and exercise, also stimulate the same airway inflammation.

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19
Q

In type I hypersensitivity, how is systemic anaphylaxis caused?

A

Exposure to allergen may cause the rapid release of vasoactive amines from mast cells and basophils as well as a flood of cytokines, resulting in the contraction of smooth muscle in the vasculature and vasodilation of capillary endothelium.

Blood pressure decreases, resulting in vascular shock.

In addition, the release of mediators increases the contraction of smooth muscles in the bronchi and bronchioles of the respiratory tract, making breathing difficult.

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20
Q

What does allergen testing assess?

A

Assess type I hypersensitivities to various potential allergens.

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21
Q

On which side of the arm is allergen testing typically performed?

A

Ventral (anterior) side of arm.

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22
Q

In an allergen test, a grid is marked on the ventral side of the arm and small quantities of substances to be tested are injected into the dermis. What indicates a positive reaction?

A

Redness and swelling within 20-30 minutes after exposure to the allergen.

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23
Q

Type II Hypersensitivity

A

> Specific Abs for cell tissue Ags may deposit in tissues and cause injury by inducing local inflammation.

> IgG and IgM Abs activate the complement system by the classical pathway, resulting in the production of complement byproducts that recruit leukocytes and induce inflammation.

> IgG Abs bind to neutrophil and macrophage Fc receptors (FcRs) and activate these leukocytes, resulting in proinflammatory response.
- ROS and lysosomal enzymes released damage the adjacent tissues.

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24
Q

What are the 3 effector mechanisms for type II hypersensitivity reactions?

A

(A) Abs opsonize cells and may activate complement and lead to phagocytosis of the cells through phagocyte FcR or CR1 for C3b.

(B) Complement byproducts C3a and C5a are chemotactic for leukocytes and recruit leukocytes.

(C) Abs specific for cell receptors for hormones or neurotransmitters:

  • may stimulate the activity of the thyroid-stimulating hormone receptors even in the absence of the hormone causing hyperthyroidism (Graves’ disease)
  • may inhibit binding of acetylcholine neurotransmitter to ACh receptor causing myasthenia gravis.
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25
Q

Type III Hypersensitivity

A

> Ab-Ag complexes may be formed in the circulation and deposited in blood vessels and other sites.

> These immune complexes induce vascular inflammation, and subsequent ischemic damage to the tissues.

> The major mechanism triggering tissue damage is classical activation of complement and recruitment of leukocytes.

26
Q

Which type of hypersensitivity is an arthus reaction?

A

Type III Hypersensitivity Reaction.

27
Q

Type III hypersensitivity diseases are caused by the deposition of immune complexes. In these diseases, immune complexes are detected in the blood or in the tissues that are the sites of injury. List some types of immune complex diseases.

A

> Systemic lupus erythematosus – nephritis, arthritis, vasculitis
Polyarteritis nodosa – vasculitis
Post-streptococcal glomerulonephritis – nephritis
Serum sickness (clinical and experimental) – sytemic vasculitis, nephritis, arthritis
Arthus reaction (experimental) – cutaneuous vasculitis

in all of these disorders, injury is caused by complement-mediated and Fc receptor-mediated inflammation

28
Q

What is the arthus reaction?

A

Induced by subcutaneous administration of a protein Ag to a previously immunized animal; it results in the formation of immune complexes at the site of Ag injection, and a local vasculitis. (compare to the systemic vasculitis in serum sickness).

29
Q

Which type of hypersensitivity is considered T cell-mediated diseases?

A

type IV

30
Q

What are the major triggers of type IV hypersensitivity reactions?

A

Reactions are:

  • autoimmunity
  • exaggerated or persistent responses to environmental Ags
  • some microbial Ags (M. tuberculosis)
31
Q

In type IV hypersensitivity reactions the major trigger reactions are autoimmunity, exaggerated or persistent responses to environmental Ags, and some microbial Ags (M. tuberculosis). What is tissue injury caused by in type IV hypersensitivity reactions?

A

Tissue injury is caused by macrophage activation and inflammation induced by cytokines that are produced mainly by CD4 Th1 cells and Th17 cells or by killing of host cells by CD8 CTLs.

32
Q

Besides T cells playing a dominant role in causing tissue injury in type IV hypersensitivity reactions. What else may also contribute?

A

Abs and immune complexes may also contribute.

33
Q

What are 3 common autoimmune diseases that are mediated by type IV hypersensitivity reactions?

A
  • Multiple sclerosis
  • Rheumatoid arthritis
  • Type 1 diabetes
34
Q

What are 2 common inflammatory diseases that have a microbial component that cause a type IV hypersensitivity reaction?

A
  • Crohn’s disease (inflammatory Bowl Disease, IBD) has both an autoimmunity component and is likely caused by the aberrant reactions to intestine microflora.
  • The other diseases like tuberculosis are caused by reactions to microbial Ags.
35
Q

What are classical T cell-mediated inflammatory reactions also known as?

A

delayed-type hypersensitivity (DTH)

36
Q

Which type of T cells secrete cytokines that recruit and activate leukocytes to cause inflammation in type IV hypersensitivity reactions?

A

Th1 and Th17

37
Q

What is the tissue injury a result of in classical T cell-mediated inflammatory reactions?

A

Results from the products of the recruited and activated neutrophils and macrophages, such as lysosomal enzymes, reactive oxygen species, nitric oxide, and proinflammatory cytokines.

Inflammation associated with T cell-mediated diseases is typically chronic

38
Q

What are many organ-specific autoimmune diseases caused by the interaction of?

A

Autoreactive T cells with self Ags, leading to cytokine release and inflammation.

39
Q

What is delayed-type hypersensitivity (DTH)?

A

An injurious cytokine-mediated inflammatory reaction resulting from the activation of T cells, particularly CD4 T cells.

the reaction is called delayed because it typically develops 24-48 hours after Ag challenge

40
Q

True or False:

Humans may be sensitized for DTH reactions by microbial infection (TB), by contact sensitization (poison ivy), or immunization (diphtheria toxin/Tetanus toxin).

A

True

41
Q

What kind of reaction is elicited by purified protein derivative (PPD), a protein antigen of Mycobacterium tuberculosis?

A

DTH reaction, called the tuberculin reaction.

42
Q

What is the involvement of cytokines in granulomatous inflammation?

A

Cytokines are involved in the generation of Th1 cells, activation of macrophages, and recruitment of leukocytes.

PROLONGED REACTIONS of this type lead to the formation of granulomas.

43
Q

What do TB granulomas from a patient with TB contain?

A
  • activated macrophages
  • multinucleate giant cells
  • lymphocytes (primary T cells)

in some granulomas, there may be a central area of necrosis

44
Q

What is the mechanism of contact dermatitis caused by poison ivy?

A
  • Pentadecacatechol molecules + skin protein –> pentadecacatechol molecules combined with skin proteins.
  • 7-10 days (no dermatitis - primary contact): T cells sensitization step –> T memory cells immune response -(1-2 days: secondary contact)-> many active T cells disease –> dermatitis.
45
Q

Initiation of Response

A
  • Shortly after exposure to Ag, resident MAST CELLS initiate cellular recruitment.
  • Released TNF recruits neutrophils, which in turn signal to activate tissue macrophages and circulating monocytes.
  • IFN-gamma produced by local NK cells and gamma-delta T cels further activates resident tissue DCs.
  • Within minutes to hours, activated Ag-loaded DCs migrate to peripheral LNs via the lymphatic channels.
46
Q

Production of Ag-Specific T cells in Developing Granuloma

A
  • Ag-loaded DCs travel to local LDs and initiate a adaptive T cell response.
  • DCs produce IL-12 and prsent Ag to naive CD4 T cells.
  • Under the influence of iL-12, naive CD4 cells differentiate into Th1 cells.
  • Activated Th1 T cells secrete IL-2, which promotes T-cell survival and proliferation, leading to expansion of the population of Ag-specific Th1 cells.
47
Q

Formation of Mature Granuloma

A
  • Within hours to days after Ag exposure, ACTIVATED Th1 cells home to the tissue.
  • If the source of Ags is not eradicated, INFLAMMATION will PERSISTS.
  • Th1 CD4 T cells and activated macrophages by IFN-gamma which leads to production of TNF.
  • IFN-gamma and TNF further stimulate macrophages.
  • Over the course of several days to weeks a MATURE GRANULOMA is formed.
48
Q

What hormone is used as an anti-inflammatory agent?

A

corticosteroids

49
Q

What are the principles of immunotherapy?

A

> Anti-Inflammatory agents (corticosteroids).

> Depletion of cells and antibodies (anti-CD20 Ab for B cells).

> Anti-cytokine therapies (anti-TNF Ab).

> Agents that inhibit cell-cell interactions and leukocyte migration (anti-CD40L).

> Intravenous IgG

> Regulatory T cell-based therapies (expand and activate Treg cells in culture and transfer them back to the patients).

50
Q

What are the characteristics of systemic lupus erythematosus?

A

> SLE is the prototypic immune complex-mediated disease (type II hypersensitivity).

> The principal clinical manifestations are rashes, arthritis, and glomerulonephritis.

> Many different auto-Abs are found. The most frequent are anti-DNA Abs.

> Immune complexes formed from these auto-Abs and their specific Ags are responsible for glomerulonephritis, arthritis, and vasculitis involving small arteries.

> The principal diagnostic test for the disease is the presence of anti-nuclear Abs.

51
Q

What is systemic lupus erythematosus (SLE)?

A

Prototypic immune complex-mediated disease (type II hypersensitivity).

52
Q

What are the principle clinical manifestations of SLE?

A
  • rashes
  • arthritis
  • glomerulonephritis
53
Q

What are the most frequent auto-Abs found to be the cause of systemic lupus erythematosus (SLE)?

A

anti-DNA Abs

54
Q

What are the immune complexes formed from anti-Abs and their specific Ags in patients with systemic lupus erythematosus (SLE) responsible for causing?

A
  • glomerulonephritis
  • arthritis
  • vasculitis involving small arteries
55
Q

What is the principle diagnostic test for the disease, SLE?

A

presence of anti-nuclear Abs

56
Q

What are the characteristics of rheumatoid arthritis (RA)?

A

> RA is an inflammatory disease involving small and large joints.

> Mediated by mixed type II/III hypersensitivity reactions.

> Th1 cells, Th17 cells, activated B cells, plasma cells, and macrophages are involved.

> Inflammation of the synovium associated with destruction of the joint cartilage and bone.

> Patients frequently have circulating IgM or IgG that react with the Fc of their own IgG molecules.

> These auto-Abs are called rheumatoid factors, and their presence is used as a diagnostic test for RA.

57
Q

Which cell types are involved in rheumatoid arthritis (RA)?

A
  • Th1 cells
  • Th17 cells
  • activated B cells
  • plasma cells
  • macrophages
58
Q

What types of hypersensitivity reactions mediate rheumatoid arthritis (RA)?

A

mixed type II/III hypersensitivity

59
Q

What type of Abs are found circulating in patients with rheumatoid arthritis (RA)?

A

Patients frequently have circulating IgM or IgG that react with the Fc of their own IgG molecules.

60
Q

What is RA?

A

Inflammatory disease involving small and large joints.

61
Q

Patients with RA frequently have circulating IgM or IgG that react with the Fc of their own IgG molecules. What type of diagnostic test is used for RA?

A

These auto-Abs are called rheumatoid factors, and their presence is used as a diagnostic test for RA.

62
Q

The pathogenesis of multiple sclerosis, type 1 diabetes mellitus, and inflammatory bowel disease are not written out in words in the lecture slides. Need to look at the figures and draw them out.

A

Slides 36-39

Keep working hard!!

Immunology - Unit 4 - Zach H. (5 decks)

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