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Pathology > Hypersensitivity, Autoimmunity and Immunodeficiency Part 1 > Flashcards

Hypersensitivity, Autoimmunity and Immunodeficiency Part 1 Flashcards

1
Q

what are the pathologic immune responses

A
  • autoimmunity
  • reactions against microbes
  • reactions against environmental antigens
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2
Q

what is autoimmunity

A

-body reacts to self antigen; lost ability to have self tolerance; react against microbes. Normal immune response to microbes is for Abs to remove them so you don’t get an infectious disease. If you have hyper reaction to those if causes inflammation and a disease process instead of a normal rxn

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3
Q

autoimmunity caused by

A
  • loss of self tolerance

- autoimmune diseases

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4
Q

immune complex formation with deposition in tissue leading to

A

inflammatory response

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5
Q

name an example of immune complex formation with deposition into tissue

A

post-streptococcal glomerulonephritis - can develop into kidney failure

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6
Q

what do T-cell responses lead to

A

severe inflammation with granuloma formation (ie. Tuberculosis)

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7
Q

T-cell responses can lead to cross-reactivity to

A 
host tissue (ex. Rheumatic heart disease)
-T-cells responses you get Abs that are formed against the strep, but cross react with heart valve
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8
Q

T-cell recognition of virus in hepatocyte leading to damage to what

A

liver cell in hepatitis (ie. viral hepatitis)

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9
Q

tissue injury caused by

A

antibodies, effector T lymphocytes and other effector cells

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10
Q

what type of disease do environmental antigens cause

A
  • chronic, debilitating diseases which are difficult to treat (ex. bronchial asthma)
  • immune mediated inflammatory diseases
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11
Q

what are the different hypersensitivity diseases

A
  1. immediate type I hypersensitivity
  2. antibody-mediated Type II hypersensitivity
  3. immune complex-mediated type III hypersensitivity
  4. T-cell mediated type IV hypersensitivity
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12
Q

what is type I hypersensitivity

A

-anaphylaxis, allergies, bronchial asthma

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13
Q

what is type I hypersensitivity caused by

A

IgE production leads to immediate release of vasoactive amines and other mediators from mast cells and basophils with subsequent recruitment of inflammatory cells with late phase rxn

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14
Q

type I hypersensitivity is characterized by

A

-vascular dilation, edema, smooth muscle contraction, mucus production, inflammation

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15
Q

type 1 hypersensitivity has 2 phase reactions, what are they

A
  1. rapid response in 5-30 mins

2. late phase response in 2-24 hrs

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16
Q

what does the rapid phase response cause

A

-vasodilation, edema and smooth muscle spasms

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17
Q

the rapid response phase is mediated by

A

preformed granule spasm

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18
Q

the late phase response is found in what % of the population

A

50%

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19
Q

the late phase response is characterized by

A

-infiltration of tissue by monocytes, eosinophils, basophils and PMN’s

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20
Q

type I hypersensitivity is associated with what type of reactions

A

allergies or allergic rxns

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21
Q

what is the mechanism of type I hypersensitivity

A
  • environmental antigens stimulate strong Th2 responses and IgE production in the genetically susceptible
  • IgE binds to Fc receptors of mast cells and re-exposure to antigen leads to cross-linking of the IgE and FcERI with activation of mast cell and release of mediators such as histamine, proteases and other granule contents; prostaglandines, leukotrienes and cytokines
  • mediators cause immediate vascular and smooth muscle rxn and the late phase inflammatory reaction
  • manifestation may be local or systemic and range from rhinitis to fatal anaphylaxis
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22
Q

see table of action of mast cell mediators in type 1 hypersensitivity

A

see table of action of mast cell mediators in type 1 hypersensitivity

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23
Q

what is type II hypersensitivity associated with

A
  • autoimmune hemolytic anemia

- Goodpasure syndrome

24
Q

type II hypersensitivity is associated with the production of

A

IgG and IgM which bind antigen on target cell or tissue with phagocytosis or lysis of target cell by activated complement or Fc receptors with recruitment of leukocytes

25
Q

type II hypersensitivity causes

A
  • phagocytosis and lysis of cells with inflammation

- there may be functional derangement without tissue or cell injury

26
Q

there are 2 types of hypersensitivity, what are they

A
  1. lysis/phagocytosis of cell

2. organ and tissue look normal under microscope, but not functioning properly

27
Q

how do antibodies opsonize cells in type II hypersensitivity

A

with or w/o complement proteins and target these cells for phagocytosis by macrophages which express receptors for the Fc tails of IgG and complement proteins destroying the target cells

28
Q

where do antibodies and immune complex deposit

A
  • in tissue or blood vessels
  • elicit an acute inflammatory reaction by activating complement w/ release of breakdown products or by engaging Fc receptors and leukocytes leading to tissue damage
29
Q

where do antibodies bind to

A

cell surface receptors or essential molecules leading to functional derangements such as inhibition or unregulated activation w/o injury

30
Q

what are the type II hypersensitivity diseases

A
  • autoimmune hemolytic anemia
  • autoimmune thrombocytopenia purpura
  • pemphigus vulgaris
  • vasculitis caused by ANCA
  • goodpasture syndrome
  • acute rheumatic fever
  • myasthenia gravis
  • Graves disease (hyperthyroidism)
  • Insulin resistant diabetes
  • Pernicious anemia
31
Q

Type III hypersensitivity occurs in what diseases

A
  • systemic lupus erythematosis
  • some forms of glomerulenophritis
  • serum sickness
  • arthus reaction
32
Q

how does type III hypersensitivity occur

A

-deposition of antigen-antibody complexes with activation of complement, recruitment of leukoctyes by complement products and Fc receptors with release of enzymes and other toxic molecules

33
Q

what can type III hypersensitivity cause

A

-inflammation, necrotizing vasculitis and fibrinoid necrosis

34
Q

tissues most affected by type III hypersensitivity are what

A

-kidney, joints, skin, heart, serosal surfaces and small blood vessels

35
Q

what initiates the immune complex mediated by type III hypersensitivity

A

-antigen-antibody complex deposition initiates acute inflammation via complement activation and accumulation of PMN’s

36
Q

what factors are involved in immune complex mediated type III hypersensitivity

A
  • endogenous antigens

- exogenous antigens

37
Q

where may immune complex mediated type III hypersensitivity rnxs form

A
  • in circulation or form in situ

- systemic vs. local rxns

38
Q

what is phase 1 of systemic type III hypersensitivity rxns

A
  • serums sickness 5 days after administration of non human sera antibodies
  • antibodies form and bind with antigen in sera in first phase
39
Q

what is the second phase of systemic type III hypersensitivity

A

-second phase complexes are deposited depending on size of complex and state of mononuclear phagocyte system

40
Q

what is the 3rd phase of systemic type III hypersensitivity

A

third phase inflammatory reaction at site of deposition after ~ 10 days

41
Q

what factors affect deposition of complexes in type III hypersensitivity

A
  • size of the complex (large complexes form in antibody excess, small complexes form in antigen excess and are more dangerous)
  • charge
  • valence
  • aviditiy of antibody
  • affinity of antigen for tissues
  • 3-D architecture of complex
  • hemodynamics
42
Q

what are the diseases of type III hypersensitivity

A
  • systemic lupus erythematosus
  • poststreptococcal glomerulonephritis
  • polyarteritis nodosa
  • reactive arthritis
  • serum sickness
  • arthus reaction experimental disorder
43
Q

type III HR are dominated by what

A

acute necrotizing vasculitis, microthrombi, and superimposed ischemic necrosis with acute inflammation of the affected organs

  • the necrotic vessel wall has a smudgy eosiniphilic appearance called fibrinoid necrosis caused by protein deposition
  • immune complexes can be seen in the tissues in the vascular wall
  • if exposure is limited, lesions heal but can become chronic if antigen exposure persists
44
Q

what is type IV hypersensitivity reactions

A

T-Cell Mediated Hypersensitivity

45
Q

what are the two types of T-cell reactions capable of causing tissue injury and disease

A
  1. delayed-type hypersensitivity initiated by CD4+T cells

2. direct cell cytotoxicity, mediated by CD8+T cells which are responsible to the tissue damage

46
Q

what is the delayed-type hypersensitivity

A
  • initiated by CD4+T cells
  • TH-1 type CD4+ T cells secrete cytokines recruiting other cells especially macrophages which are the major effector cells
47
Q

type IV HR are involved with what diseases

A
  • contact dermatitis, multiple sclerosis, type 1 diabetes, transplant rejection and tuberculosis
  • peripheral neuropathy, Guillain-Barre syndrome, inflammatory bowel disease (ie. Chron’s disease)
48
Q

what is the mechanism of type IV hypersensitivity

A
  • activated T lymphocytes lead to release of cytokines and macrophage activation
  • activated T lymphocytes mediate cytotoxicity
  • perivascular cellular infiltrates, edema, cell, destruction, and granuloma formation
49
Q

what is the classic delayed-type IV hypersensitivity

A
  • is the tuberculin rxn which peak at 24 to 72 hrs
  • histologically there is perivascular cuffing by CD4+T cells and macrophages
  • secretion of cytokines leads to microvascular permeability leading to dermal edema, fibrin deposition and tissue induration
50
Q

in type IV HR, TB antigens are processed by what

A

macrophages

  • APC presents Ag to CD4+T cell (class II MHC Ag)
  • sensitized CD4 + T cell remains in circulation
  • re-exposure leads to activation, amplification and recruitment of macrophages
51
Q

what is contact dermatitis (poison ivy)

A

-vesicular dermatitis due to pentadecylcatechol (urushiol) exposure

52
Q

type IV HR is mediated by what cell

A
  • T cell mediated cytotoxicity

- sensitized CD8 + T cells directly kill Ag bearing target cell (class I MHC Ag)

53
Q

cytotoxic T cells are important to resist

A

viral infection

-important tumor immunity

54
Q

what is the killing mechanism of type IV HR

A
  • perforin-granzyme dependent
  • leads to osmotic lysis via perforin
  • leads to apoptosis via granzyme
55
Q

what happens n delayed-type IV hypersensitivity

A

CD4+ T cells are activated by exposure to a protein antigen and differentiate in TH-1 effector cell

  • next exposure to the antigen leads to secretion of cytokines
  • IFN-Y activates macrophages to cause tissue damage and promote fibrinosis and TNF promotes inflammation
56
Q

what happens in T-cell mediated cytotoxicity

A

CD8+ cytotoxic T lymphocytes specific for an antigen recognize cells expressing the target antigen and kill these cells
-CD8+ T cells also secrete IFN-Y

Pathology (18 decks)

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