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Immuno Exam 3 > Hypersensitivity Disorders > Flashcards

Hypersensitivity Disorders Flashcards

1
Q

___________ (or allergy) is an exaggerated immune response harmful to the organism itself.

A

Hypersensitivity

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2
Q

T/F. The phenomenon of hypersensitivity was established more than a century ago. In 1963, Patrick Gell and Robin Coombs produced classification of hypersensitivity.

A

True

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3
Q

The classification of hypersensitivity distinguishes four types of reactions based on:

    • ________-________ effector mechanisms
    • ________-________ effector mechanisms
A

Antibody-mediated

Cell-mediated

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4
Q

In hypersensitivity classification, antibody-mediated effector mechanisms include Type I, II, and II. These types correspond to defenses against (EXTRACELLULAR/INTRACELLULAR) pathogens.

A

Extracellular

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5
Q

In hypersensitivity classification, cell-mediated effector mechanisms include Type IV. This type corresponds to defense against (EXTRACELLULAR/INTRACELLULAR) pathogens.

A

Intracellular

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6
Q

Clinical manifestations of immediate type I hypersensitivity result form the actions of mediators secreted by the _______ cells.

A

Mast

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7
Q

Hypersensitivity type ____ Abs against cell and tissue Ags may cause tissue injury and disease.

A

II

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8
Q

In immune complex diseases (type _____ hypersensitivity), Abs may bind to circulating Ags to form immune complexes, which deposit in vessels, leading to inflammation in the vessel wall (vasculitis).

A

III

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9
Q

Hypersensitivity type ____ is T cell-mediated diseases which result from inflammation caused by cytokines produced by CD4+ Th1 and Th17 cells, or killing of host cells by CD8+ CTLs.

A

IV

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10
Q

Immediate type _____ hypersensitivity is a type of pathologic reaction that is caused by the release of mediators from mast cells. This reaction is most often triggered by the production of ____ Ab against environmental Ags and the binding of ____ to mast cells in various tissues.

A

I
IgE
IgE

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11
Q

______ refers to the genetic tendency to develop allergic diseases. Individuals with a strong propensity to develop allergic reactions are said to be ______.

A

Atopy

Atopic

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12
Q

Type I hypersensitivity reactions is controlled by the binding of IgE Abs to _______ located on the membrane of mast cells, basophils, and eosinophils.

A

FceR1

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13
Q

The IgE-FceR1 binding has high affinity for IgE. Most of the IgE produced following initial contact (priming) with Ag becomes ‘_______’ on the surface of mast cells and eosinophils. Upon a second contact with Ag, the Ag-Ab reactions occurs predominantly on the mast cell and basophil membrane.

A

Fixed

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14
Q

Put the following events in the development of immediate hypersensitivity (Type I) reactions in order:

A. Binding of the IgE to Fc receptors of mast cells.

B. Release of mediators by mast cell after secondary exposure to the Ag and cross-linking of the membrane-bound IgE by Ags.

C. Production of IgE after activation of Th2 cells by primary exposure to allergens.

A
  1. C
  2. A
  3. B
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15
Q

The most important mediators produced by mast cells are vasoactive amines, proteases, prostaglandins and leukotrienes, and cytokines. The major amine, ________, causes the dilation of small blood vessels and increases vascular permeability. Damage to local tissues may be caused by _______.

A

Histamine

Proteases

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16
Q

_________ cause vascular dilation, and _________ stimulate prolonged smooth muscle contraction. ________ induce local inflammation (the late-phase reaction).

A

Prostaglandins
Leukotrienes
Cytokines

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17
Q

______ cell mediators are responsible for acute vascular and smooth muscle reactions and inflammation, the hallmarks of immediate hypersensitivity.

A

Mast

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18
Q

The immediate vascular and smooth muscle reaction to allergen develops within minutes after challenge. Morphology of the immediate reaction is characterized by ________, ________, and ________.

A

Vasodilation
Congestion
Edema

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19
Q

The ______-_____ reaction develops 2 to 24 hours later. It is characterized by an inflammatory infiltrate rich in eosinophils, neutrophils, and T cells.

A

Late-phase

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20
Q

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

A

Asthma

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21
Q

In asthma, these inflammatory mediators cause the loosening of tight junctions in the ________ epithelium, increased capillary permeability, and spastic contraction of smooth muscle surrounding the _______. This temporarily decreases the size of the ________ lumen, resulting in shortness of breath.

A

Bronchiole
Bronchi
Bronchial

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22
Q

Non-Immunologic stimuli such as cold, viral infections, and exercise, also stimulate the airway inflammation and _________.

A

Bronchospasms

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23
Q

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 _________ of capillary endothelium. Blood pressure _______, resulting in vascular shock. (Anaphylaxis)

A

Vasodilation

Decreases

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24
Q

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

A

Mediators

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25
Q

In allergen testing, these tests are based on ______ hypersensitivity reactions to various potential allergens. Testing is often performed on the ventral side of the arm. A grid is marked and small quantities of standardized substances to be tested are injected into the dermis. Positive reactions are indicated as redness and swelling within 20 to 30 minutes after exposure to the allergen.

A

Type I

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26
Q

In Type II hypersensitivity, Abs specific for cell and tissue Ags may deposit in tissues and cause injury by inducing local inflammation. Abs (_____ and _____) activate the complement system by the _______ pathway, resulting in the production of complement byproduct that recruit leukocytes and induce inflammation.

A

IgG
IgM
Classical

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27
Q

IgG antibodies bind to _______ and _______ Fc receptors and activate these leukocytes, resulting in pro inflammatory response. ______ and _______ enzymes released damage the adjacent tissues.

A

Neutrophil
Macrophage
ROS
Lysosomal

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28
Q

In type II hypersensitivity, Ags are (SOLID/SOLUBLE).

A

Solid

29
Q

In type III hypersensitivity, Ags are (SOLID/SOLUBLE).

A

Soluble

30
Q

In type III hypersensitivity, 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 _______ damage to the tissues.

A

Ischemic

31
Q

In type III hypersensitivity, the major mechanism triggering tissue damage is _______ activation of complement.

A

Classical

32
Q

Type III hypersensitivity is mediated by the deposition of Ag-Ab complexes. The complexes fix complement to release the anaphylatoxin products _____ and _____. Inflammatory cells (basophils and especially neutrophils) release _______ _______.

A

C3a
C5a
Vasoactive amines

33
Q

Type III hypersensitivity reactions are caused by Ab-Ag complexes. When significant quantities of such immune complexes are formed, they can deposit in tissues leading to tissue damage is mediated by:

    • ________ activation
    • ______ cell degranulation
    • _______ chemotaxis
    • _______ caused by immune cells
A

Complement
Mast
Neutrophil
Inflammation

34
Q

Type III hypersensitivity diseases are caused by the deposition of immune complexes. In the diseases, immune complexes are detected in the _______ or in the _______ that are the sites of injury. In all the disorders, injury is caused by complement-mediated and Fc-receptor-mediated inflammation.

A

Blood

Tissues

35
Q

The _______ reaction (disease of type III hypersensitivity) is 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.

A

Arthus

36
Q

The major causes of T cell-mediated hypersensitivity (type IV) reactions are ________ and exaggerated or persistent responses to environmental Ags. Tissue injury also may accompany T cell responses to microbes (M. tuberculosis).

A

Autoimmunity

37
Q

In different T cell-mediated diseases, tissue injury is caused by ________ induced by cytokines that are produced mainly by CD4+ Th1 cells and Th17 cells or by killing of host cells by CD8+ CTLs.

A

Inflammation

38
Q

Type IV hypersensitivity (Delayed Type Hypersensitivity, DTH) is caused by activated _____ cells. The _________ phase of DTH can be caused by intracellular pathogens.

A

Th1

Sensitization

39
Q

Upon re-encounter with Ag, the Ag-specific Th1 clones undergo further clonal expansion and secretion of ______ and _____ which activate macrophages causing macrophage-dependent tissue damage.

A

IFN-y

TNF-B

40
Q

Unlike type I, II, and III reactions that can be transferred by serum containing Abs, passive transfer of type IV requires the transfer of antigen-specific _____ clones that orchestrate the macrophage response.

A

Th1

41
Q

In immune-mediated inflammation, _____ and _____ cells secrete cytokines that recruit and activate leukocytes.

A

Th1

Th17

42
Q

Tissue injury results from the products of the recruited and activated neutrophils and macrophages, such as lysosomal enzymes, reactive oxygen species, _____ _____, and pro inflammatory cytokines.

A

Nitric oxide

43
Q

The inflammation associated with T cell-mediated diseases is typically ______.

A

Chronic

44
Q

Many organ-specific autoimmune diseases are caused by interaction of auto reactive T cells with _______, leading to cytokine release and inflammation. T cell reactions specific for microbes and other foreign Ags may also lead to inflammation and tissue injury.

A

Self-Ags

45
Q

The classical T cell-mediated inflammatory reaction is called…

A

Delayed-type Hypersensitivity (DTH)

46
Q

T/F. T cells play a dominant role in causing tissue injury but Abs and immune complexes may also contribute.

A

True

47
Q

Multiple sclerosis, rheumatoid arthritis, and type 1 diabetes are ________ disorders.

A

Autoimmune

48
Q

_______ disease, an inflammatory bowel disease, is likely caused by reactions against microbes in the intestine and may have a component of autoimmunity.

A

Crohn’s

49
Q

Delayed-type hypersensitivity (DHT) is an injurious cytokine-mediated inflammatory reaction resulting from the activation of T cells, particularly ______ T cells. The reaction is called delayed because it typically develops 24 to 48 hours after Ag challenge.

A

CD4+

50
Q

Humans may be sensitized for ______ reactions by microbial infection (TB), by contact sensitization (Poison Ivy) or immunization (diphtheria toxin/Tetanus toxin).

A

DTH

51
Q

Purified protein derivative (PPD), a protein antigen of Mycobacterium tuberculosis, elicits a DTH reaction, called the ________ reaction.

A

Tuberculin

52
Q

TB granuloma from a patient with TB. Granulomas contain activated macrophages, multinucleate giant cells, and lymphocytes (primarily T cells). In some granulomas, there may be a central area of ________. 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 mature granulomas.

A

Necrosis

53
Q

A thick layer of epithelioid macrophages prevent CD4 and CD8 effector T cells from access of the bacteria and thus allows survival of mycobacteria tuberculosis in the mature _______ for a long time.

A

Granuloma

54
Q

Systemic Lupus Erythematosus (SLE) is the prototypic immune complex-mediated disease (type _____ hypersensitivity).

A

III

55
Q

In ______, the principal clinical manifestations are rashes, arthritis, and glomerulonephritis. Many different auto-Abs are found. The most frequent are anti-DNA Abs.

A

SLE

56
Q

In SLE, immune complexes formed from these auto-Abs and their specific Ags are responsible for glomerulonephritis, arthritis, and vasculitis involving small arteries. The principle diagnostic test for the disease is the presence of _________ Abs.

A

Anti-nuclear

57
Q

(SLE) Presentation of unknown antigens by MHC molecules leads to priming of ______ T cells. These _____ T cells then help B cells in auto reactive germinal centers undergo class switching, affinity maturation and differentiation into plasma cells that secrete high levels of soluble autoantibodies of the _____ isotype.

A

CD4+
CD4+
IgG

58
Q

(SLE) These autoantibodies form immune complexes by binding auto antigens, and fix complement or engage ______ receptors on several different cell types. This can support inflammation and tissue destruction through the recruitment of inflammatory cells to tissues.

A

Fcy

59
Q

(SLE) Apoptotic cells from damaged tissues can be taken up by _________, which present novel auto antigens, supporting further priming and auto reactivity.

A

Phagocytes

60
Q

(SLE) Engagement of TLRs by environmental triggers such as viral infection or DNA damage by _______ contribute to the process by inducing the secretion of IFN-I and other cytokines, supporting lymphocyte auto reactivity as well as tissue destruction.

A

UV rays

61
Q

This is an inflammatory disease involving small and large joints. Inflammation of the synovium associated with destruction of the joint cartilage and bone.

A

Rheumatoid arthritis (RA)

62
Q

RA is mediated by mixed type _____ and _____ hypersensitivity reactions.

A

II

IV

63
Q

The cells involved in RA are Th1 cells, Th17 cells, activated B cells and _______ cells, and macrophages.

A

Plasma

64
Q

With RA, patents frequently have circulating _____ or _____ that react with the Fc of own IgG (non-immune) molecules. These auto-Abs are called rheumatoid _______, and their presence is used as a diagnostic test for RA.

A

IgM
IgG
Factors

65
Q

A type of immunotherapy is the use of anti-inflammatory agents like ________.

A

Corticosteroids

66
Q

A type of immunotherapy is the use of depletion of cells and antibodies, like ________ Ab for B cells.

A

Anti-CD20

67
Q

A type of immunotherapy is the use of agents that inhibit cell-cell interactions and leukocyte migration (_______).

A

anti-CD40L

68
Q

A type of immunotherapy is intravenous _____.

A

IgG

69
Q

A type of immunotherapy is the use of regulatory T Cell-based therapies, such as expanding and activating _____ cells in culture and transferring them back to the patients.

A

Treg

Immuno Exam 3 (6 decks)

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