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Immunology Final Exam - AH > Chapter 19 - Hypersensitivity > Flashcards

Chapter 19 - Hypersensitivity Flashcards

1
Q

what is characteristic of type II hypersensitivity?

A

Ag in tissue, solid Ag (Ab against tissue)

ex. pancreas

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2
Q

What is involved in type 3 hypersensitivity?

what does it lead to?

A

immune complex diseases, soluble Ag in circulation, complement system

vasculitis

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3
Q

What are some examples of type 4 hypersensitivity?

what does it result from?

A

infection, environmental Ag, post vaccination
cell-mediated

inflammation caused by ctyokines from Th1 and Th17 cells, or CTLs

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4
Q

what is atopy?

A

genetic tendency to develop allergic diseases

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5
Q

describe the sequence of events in the development of immediate hypersensitivty

A

activation of Th2 cells and IgE production in response to Ag
binding of IgE to FcERI receptors of mast cells
exposure to Ag, cross-linking of bound IgE by Ag and release of mediators

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6
Q

what happens immediately after Ag exposure (1st hour)?

what is the morphology characterized as?

A

vascular and smooth muscle reaction to allergen

vasodilation, congestion, and edema

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7
Q

when does the late phase reaction develop?

how is it characterized?

A

2-24 hours

inflammatory infiltrate of eosinophils, neutrophils, and T cells

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8
Q

what are the most important mediators produced by mast cells?

A

vasoactive amines, proteases, prostaglandins, leukotrienes, and cytokines

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9
Q

what causes dilation of small blood vessels and increases vascular permeability?

A

histamine

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10
Q

what do proteases do?

A

cause damage to local tissue

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11
Q

what do prostaglandins do?

leukotrienes?

A

cause vascular dilation

stimulate prolonged smooth muscle contraction

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12
Q

what do cytokines do?

A

induce local inflammation (late-phase reaction)

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13
Q

how is type II hypersensitivity activated?

how else?

A

IgG and IgM activate the classical complement system, resulting in the production of byproducts that recruit leukocytes and induce inflammation

chemoattractants (opsonization) and phagocytosis of cells

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14
Q

what damages adjacent tissues?

A

ROS and lysosomal enzymes released

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15
Q

what binds to neutrophils and macrophage Fc receptors and activates leukocytes, resulting in proinflammatory response?

A

IgG Abs

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16
Q

what are the 3 effector mechanisms of type II?

A

1) opsonization and phagocytosis
2) Complement and Fc receptor-mediated inflammation
3) Abnormal physiological responses without cell/tissue injury

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17
Q

what type of hypersensitivity is goodpasture’s syndrome’s, the mechanism of disease and clinical manifestation?

A

type II, complement and Fc receptor mediated inflammation

nephritis, lung hemorrhage

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18
Q

what type of hypersensitivity is Grave’s syndrome’s, the mechanism of disease and clinical manifestation?

A

type II, Ab-mediated stimulation of TSH receptors

hyperthyroidism

19
Q

what type of hypersensitivity is Myasthenia gravis syndrome’s, the mechanism of disease and clinical manifestation?

A

type II, Ab inhibits Ach binding, down-regulates receptors

muscle weakness, paralysis

20
Q

what type of hypersensitivity is Pemphigus vulgaris syndrome’s, the mechanism of disease and clinical manifestation?

A

type II, Ab-mediated activation of proteases, disruption of intracellular adhesions

skin vesicles (bullae)

21
Q

what type of hypersensitivity is Pernicious anemia syndrome’s, the mechanism of disease and clinical manifestation?

A

type II, Neutralization of intrinsic factor, dec. absorption of Vit B12

anemia

22
Q

what type of hypersensitivity is Rheumatic fever syndrome’s, the mechanism of disease and clinical manifestation?

A

type II, inflammation, macrophage activation

myocarditis, arthritis

23
Q

Ab-Ag complexes of what Abs may be formed in the circulation and deposited in blood vessels and other sites

A

IgG, IgM

24
Q

what type of hypersensitivity is Systemic lupus erythematosus syndrome, what are the clinical manifestations?

what auto-Abs are found and what is formed from them?

A

type III, rashes, arthritis, glomerulonephritis

anti-DNA Abs, immune complexes formed responsible for effects

25
Q

what type of hypersensitivity is Rheumatoid Arthritis syndrome, the mechanism of disease and clinical manifestation?

A

mixed type II and III
Th1 and Th17 cells, activated B, plasma cells and macrophages
involves small and large joints where inflammation of the synovium and destruction of joint cartilage and bone occurs

26
Q

in RA, what kind of Abs react with what in their own body?

what are these auto-Abs called?

A

IgG and IgM react with the Fc of their own IgG molecules

rheumatoid factors

27
Q

what type of hypersensitivity is polyarteritis nodosa syndrome, the clinical manifestation and what Ab specificity does it have?

A

type III, vasculitis

microbial Ags ie hep B

28
Q

what type of hypersensitivity is Post-streptococcal glomerulonephritis syndrome, the clinical manifestation and what Ab specificity does it have?

A

type III, nephritis, streptococcal cell wall Ag

29
Q

what type of hypersensitivity is serum sickness syndrome, the clinical manifestation and what Ab specificity does it have?

A

type III, systemic vasculitis, nephritis, arthritis

protein Ag

30
Q

what type of hypersensitivity is Arthus reaction syndrome, the clinical manifestation and what Ab specificity does it have?

A

type III, cutaneous vasculitis

protein Ag

31
Q

What are the major causes of T-cell mediated hypersensitivity reactions?

A

autoimmunity and exaggerated/persistent responses to environmental Ags

32
Q

tissue injury also may accompany T cell response to what?

A

microbes (M. tuberculosis)

33
Q

what type of hypersensitivity is multiple sclerosis, the clinical manifestation and what specificity of pathogenic T cells does it have?

A

type IV, demylenation in CNS, motor and sensory dysfunction

myelin proteins

it is an autoimmune disorder

34
Q

what type of hypersensitivity is Type I diabetes, the clinical manifestation and what specificity of pathogenic T cells does it have?

A

type IV, impaired glucose metabolism, vascular disease

pancreatic islet Ags

autoimmune disorder

35
Q

what type of hypersensitivity is Crohn’s disease, the clinical manifestation and what specificity of pathogenic T cells does it have?

A

inflammation of bowel wall, abdominal pain, diarrhea, hemorrhage

g.i. microbes

36
Q

what type of hypersensitivity is contact sensitivity, the clinical manifestation and what specificity of pathogenic T cells does it have?

A

type IV, DTH reaction in skin and rash

modified skin proteins

37
Q

what type of hypersensitivity is chronic infections, the clinical manifestation and what specificity of pathogenic T cells does it have?

A

Chronic inflammation

microbial proteins

38
Q

what is DTH?

when does it occur?

give an example

A

injurious cytokine-mediated inflammatory reaction resutling from act. of CD4 T cells

occurs 24-48 hours after Ag challenge
ex: PPD Ag to TB

39
Q

how are granulomas formed?

A

prolonged reactions in which cytokines are involved in the generation of Th1 cells, activation of macrophages and recruitment of leukocytes

40
Q

what are the immunotherapy methods?

A

anti-inflammatory agents (corticosteroids) INHIBITS NF-KB
depletion of cells and Abs (anti-CD20 Ab for B cells)
Anti-cytokine (anti-TNF Ab)
Inhibitory agents of cell-cell interactions and Leukocyte migration (anti-CDL)
Treg therapies

41
Q

what does anti-p40 do?

A

blocks Th1 and Th17 responses

42
Q

what does IL-2R do?

A

block T cell proliferation

43
Q

what do inhibitors of calcineurin, Jaks and other kinases do?

A

inhibit signaling

44
Q

Immediate type I involves what kind of responses?

what does it result from?

A

allergic

mediators secreted by mast cells

Immunology Final Exam - AH (6 decks)

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