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SFM Exam 2 > Hypersensitivity Disorders Caused by Immune Responses > Flashcards

Hypersensitivity Disorders Caused by Immune Responses Flashcards

1
Q

Hypersensitivity Reations

A

immune responses that cause tissue injury

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2
Q

Hypersensitivity reactions may arise from:

A

(1) uncontrolled or abnormal responses to non-self Ags

(2) autoimmune responses against self-Ags

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3
Q

What are the 3 mechanisms of desensitization in type I?

A
  • IgG blocking antibodies
  • Regulation
  • Immune deviation
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4
Q

IgG Blocking Antibodies

A
  • repeated exposure to desensitizing allergens results in the development of IgG Abs which compete with IgE for allergen binding
  • leads to prevention of IgE-dependent activation of mast cells via FcεR1 receptors
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5
Q

Regulation

A
  • repeated exposure to desensitizing allergens induces Treg cells
  • allergen activated Treg cells produce anti-inflammatory IL-10 and TGF-β which inhibit migration and tissue infiltration by eosinophils and prevent their release of inflammatory mediators
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6
Q

Immune Deviation

A
  • repeated exposure to desensitizing allergens induces a shift from Th2 to Th1 CD4 cells that results in the generation of cytokines (IFN-γ) that inhibits IgE production
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7
Q

What are the 6 major diseases mediated by Type II Hypersensitivity?

A

My Rat Has The Good Genes

  • Myasthenia gravis
  • Rheumatic fever
  • autoimmune Hemolytic anemia
  • autoimmune Thrombocytopenic purpura
  • Goodpasture’s syndrome
  • Graves disease
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8
Q 
(TYPE II)
Graves Disease 
(1) Target Antigen
(2) Mechanisms of disease
(3) Clinicopathologic manifestations
A

(1) TSH receptor
- Abs activate the TSH receptor leading to over production of TSH
(2) Antibody mediated stimulation of TSH receptors
(3) Hyperthyroidism

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9
Q 
(TYPE II)
Myasthenia Gravis 
(1) Target Antigen
(2) Mechanisms of disease
(3) Clinicopathologic manifestations
A

(1) Ach receptor
- Abs block binding of Ach to receptor meaning muscles don’t get stimulated
(2) Ab inhibits Ach binding, down-modulates receptors
(3) Muscle weakness, paralysis

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10
Q 
(TYPE II)
Rheumatic Fever 
(1) Target Antigen
(2) Mechanisms of disease
(3) Clinicopathologic manifestations
A

(1) Streptococcal cell wall antigen; Ab cross-reacts with myocardial antigen
- Abs accidentally target proteins on our own cell membrane b/c look like proteins on foreign strep cells
(2) Inflammation (due to cytokine mediated response), macrophage activation
(3) Myocarditis, arthritis

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11
Q 
(TYPE II)
Goodpasture's Syndrome
(1) Target Antigen
(2) Mechanisms of disease
(3) Clinicopathologic manifestations
A

(1) Abs bind to intrinsic Ags on collagen of basement membrane in glomeruli in kidneys or alveoli in lungs
(2) Complement and Fc receptor mediated inflammation
(3) Nephritis, lung hemorrhage

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12
Q 
(TYPE II)
Autoimmune (idiopathic) Thrombocytopenic Purpura
(1) Target Antigen
(2) Mechanisms of disease
(3) Clinicopathologic manifestations
A

(1) Platelet membrane proteins (gbIIb/llla integrin)
- proteins mediate aggregation of platelets to form “plug” at site of injury
(2) Opsonization and phagocytosis of platelets
- IgG autoantibodies bind to gbIIb/IIIa receptor and target platelet/Ab complex for destruction in spleen
(3) Bleeding, purpura
- decreased platelets in blood so harder for bleeding to stop

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13
Q 
(TYPE II)
Autoimmune Hemolytic Anemia
(1) Target Antigen
(2) Mechanisms of disease
(3) Clinicopathologic manifestations
A

(1) Erythrocyte membrane proteins (Rh blood group antigens)
(2) Opsonization and phagocytosis of erythrocytes
(3) Hemolysis, anemia

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14
Q

What are the 5 major diseases mediated by Type III Hypersensitivity?

A

LAPPS

  • systemic Lupus erythematosus
  • Arthus reaction
  • Polyarteritis nodosa
  • Poststreptococcal glomerulonephritis
  • Serum sickness
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15
Q

(TYPE III)
Systemic Lupus Erythematosus
(1) Antibody specificity
(2) Clincopathologic manifestations

A

(1) DNA, nucleoproteins
- self reactive B and T cells produce Abs against autoantigens (self antigens) released from DNA or nucleoproteins; leads to B and T cells producing Abs against healthy/normal DNA and nucleoproteins
(2) Nephritis, arthritis, vasculitis

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16
Q

(TYPE III)
Polyarteritis Nodosa
(1) Antibody specificity
(2) Clincopathologic manifestations

A

(1) in some cases, microbial Ags (i.e. Hep B virus surface Ag); in most cases, unknown
(2) Vasculitis

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17
Q

(TYPE III)
Poststreptococcal Glomerulonephritis
(1) Antibody specificity
(2) Clincopathologic manifestations

A

(1) Strepococcal cell wall antigen(s)
- glomeruli become inflammed after infection by strep; immune complexes form and are carried to glomerulus where they become trapped in basement membrane which leads to local inflammation and damage thus allowing for larger molecules to be excreted in urine
(2) Nephritis

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18
Q

(TYPE III)
Serum Sickness
(1) Antibody specificity
(2) Clincopathologic manifestations

A

(1) Various protein Ags
- happens when patient receives foreign serum and elicits an Ab response against foreign Ags (i.e patient w/ IV administration of a protein Ag to a previously immunized patient that leads to formation of immune complexes
(2) Systemic vasculitis, nephritis, arthritis

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19
Q

(TYPE III)
Arthus Reaction
(1) Antibody specificity
(2) Clincopathologic manifestations

A

(1) Various protein Ags

(2) Cutaneous vaculitis

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20
Q

Anti-Venom Example of Serum Sickness

A
  • bit by poisonous snake so receive serum with anti-venom Abs
  • body responds by making Abs against anti-venom Abs
  • person gets bit again by a venomous snake so gets another dose of serum with anti-venom Abs
  • Abs that were made in body in response to first dose bind and make immune complexes with anti-venom Abs (now being treated like an Ag)
  • Ab anti-venom Ab complexes causes vasculitis and tissue necrosis
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21
Q

What are the 7 major diseases mediated by Type IV Hypersensitivity?

A
  • Multiple Sclerosis
  • Rheumatoid Arthritis
  • Type 1 DM
  • Crohns Disease
  • Psoriasis
  • Contact Sensitivity (ex. poison ivy, drug rxn)
  • Chronic Infections (ex. Tuberculosis)
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22
Q

(TYPE IV)
Multiple Sclerosis
(1) Specificity of Pathogenic T Cells
(2) Clincopathologic manifestations

A

(1) Myelin proteins

(2) Demyelination in the CNS, sensory and motor dysfunction

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23
Q

(TYPE IV)
Rheumatoid Arthritis
(1) Specificity of Pathogenic T Cells
(2) Clincopathologic manifestations

A

(1) Unknown antigens in joint

(2) Inflammation of synovium and erosion of cartilage and bone in joints

24
Q

(TYPE IV)
Type 1 DM
(1) Specificity of Pathogenic T Cells
(2) Clincopathologic manifestations

A

(1) Pancreatic islet antigens attacked by CTLS

(2) Impaired glucose metabolism, vascular disease

25
Q

(TYPE IV)
Crohns Disease
(1) Specificity of Pathogenic T Cells
(2) Clincopathologic manifestations

A

(1) Unknown, maybe role of intestinal microbes

(2) Inflammation of bowel wall (due to TH1 cells); abdominal pain, diarrhea, hemorrhage

26
Q

(TYPE IV)
Psoriasis
(1) Specificity of Pathogenic T Cells
(2) Clincopathologic manifestations

A

(1) Unknown

(2) Chronic skin inflammation

27
Q

(TYPE IV)
Contact Sensitivity (ex. poison ivy, drug rxn)
(1) Specificity of Pathogenic T Cells
(2) Clincopathologic manifestations

A

(1) Modified skin proteins
(2) DTH (delayed type hypersensitivity) reaction in skin, rash
- attack by TH1 cells

28
Q

(TYPE IV)
Chronic Infections (ex. Tuberculosis)
(1) Specificity of Pathogenic T Cells
(2) Clincopathologic manifestations

A

(1) Microbial proteins

2) Chronic inflammation (ex. granulomatous

29
Q

Type I Hypersensitivity Reactions are mediated by ___ and results from actions of mediators secreted by __ cells

A
  • IgE

- Mast

30
Q

Type I Hypersensitivity

(1) Pathologic immune mechanisms
(2) Mechanisms of tissue injury and disease

A

(1) TH2 cells, IgE antibody, mast cells, eosinophils
(2) Mast cell derived mediators (vasoactive amines, lipid mediators, cytokines); Cytokine mediated inflammation (eosinophils, neutrophils)

31
Q

Type I Hypersensitivity reactions are most often caused by ___ ___

A

Environmental Ags (allergens)

32
Q

Atophy

A
  • genetic tendency to develop allergic diseases

- individuals with a strong predisposition to develop allergic rxns

33
Q

List the steps involved in Phase I Sensitization to an Allergen

A

(1) Allergen gets picked up by APC that is in mucous membrane cell of body
(2) APC presents antigen in lymph node to naive T cell
(3) T cell bind to Ag and co-stimulatory molecule which results in T cell turning into TH2 cell via IL-4 secretion from APC, also release of IL-5 to recruit eosinophils
(4) TH2 releases IL-4 which binds to B cells and facilitates class switching from IgM to IgE
(5) IgE released from B cell binds to FcεR1 (CD23) on mast cell

34
Q

List the steps involved in Phase II Allergic Reactions (Subsequent encounter to allergen)

A

(1) Mast cells use IgE and bind to antigen of allergen which requires 2+ bound antigens to crosslink the IgE antibodies and send signal for mast cell to degranulate and release pro-inflammatory mediators (vasoactive amines, cytokines/chemokines, lipids)
(2) Release of mediators results in vascular smooth muscle contraction (results in SOB), endothelial vasodilation (results in edema and hives)

35
Q

___ is the major amine that causes dilation of small vessels and increases vascular permeability

A

Histamine

36
Q

___ cause local tissue damage

A

Proteases

37
Q

___ causes vascular dilation

A

Prostaglandins

38
Q

____ stimulate prolonged smooth muscle contraction

A

Leukotrienes

39
Q

____ induce local inflammation (the LATE PHASE RXN)

A

Cytokines

40
Q

Allergen specific immunotherapy is applied in order to:

A
  • induce peripheral T cell tolerance to allergens
  • increase the thresholds for mast cell and basophil activation by allergens
  • decrease IgE mediated histamine release by mast cells
  • generate allergen-specific inducible FoxP3+ CD4+ CD25+ Treg cells
41
Q

Effector Mechanisms of Type II Hypersensitivity

A

(1) Opsonization and Phagocytosis
- IgG opsonization of cells leads to phagocytosis of the cells thru FcγR (IgG receptor) or CR1 receptors
- neutrohpils and macrophages activated in a FcγR or CR1 dependent manner release their inflammatory mediators – ROS and lysosomal enzymes that damage adjacent tissues and cause inflammation
(2) Complement and Fc receptor mediated inflammation
- IgG and IgM can activate the CP that results in production of C3a and C5a which promote leukocyte recruitment and inflammation

42
Q

Ab-Dependent Effector Mechanisms of Type II Hypersensitivity
- Ab-Dependent Cellular Cytotoxicity (ADCC) requires what two things?

A
  • immune cells express FcγRIII on their surface

- target cells coated by Ab recognize Ags on the cell surface

43
Q

What cell expresses high levels of the FcγRIII and are regarded as the key players in ADCC?

A

NK Cells

44
Q

What 4 cells mediate ADCC?

A
  • NK cells (!!!!)
  • Macrophages
  • Neutrophils
  • Eosinophils
45
Q

Penicillin Induced Anemia

A
  • drug binds directly to RBC surface and induces an anti-drug Abs; IgG or IgM activates compliment proteins that eventually kill the RBC that is bound to penicillin
  • conditions improve when drug is discontinued
46
Q

Immune Complex-Induced Anemia

A
  • Abs form immune complexes with a drug
  • immune complexes can bind to the RBC surface via CR1
  • complement is activated on RBC surface that leads to hemolysis
  • process: IgM or IgG activates complement -> release of C3a, C4a, C5a -> recruitment of neutrophils to RBC with bound drug -> neutrophil degranulates and releases peroxidase / protease (ROS) -> killing of RBC
47
Q

Type II Hypersensitivity diseases are caused by:

A

Abs against cell/tissue Ags – Ab mediated destruction of healthy cells in specific tissues

48
Q

Autoimmune Anemias

A
  • drug induces anti-drug Abs that cross-react with an Rh Ag on RBCs
  • Ab binding to Rh Ag activates phagocytosis and complement
  • treatment may require immunosuppression or removal of immune complexes by plasmapheresis
49
Q

Type III Hypersensitivity diseases are caused by:

A

Ag-Ab complexes deposited in blood vessel walls (likely in kidneys or lungs) – leads to inflammation and tissue damage

50
Q

Type III Hypersensitivity

(1) Pathologic immune mechanisms
(2) Mechanisms of tissue injury and disease

A

(1) immune complexes of circulating antigens and IgM or IgG Abs deposited in vascular basement membrane (leads to activation of complement)
(2) complement and Fc receptor mediated recruitment and activation of leukocytes (via chemotactic activity of released C5a, C4a and C3a)

51
Q

Type IV Hypersensitivity

(1) Pathologic immune mechanisms
(2) Mechanisms of tissue injury and disease

A

(1) (a) CD4+ T cells (cytokine mediated inflammation) or (b) CD8+ CTLs (T cell mediated cytolysis)
(2) (a) macrophage activation, cytokine mediated inflammation (b) direct target cell lysis, cytokine mediated inflammation

52
Q

Type IV Hypersensitivity diseases are caused by:

A

Cell mediated immunity – T cells

53
Q

Type IV Hypersensitivity can be triggered by what 3 things?

A

(1) autoimmunity
(2) exaggerated or persistent responses to environmental Ags (ex. poison ivy)
(3) microbial Ags (ex. tuberculosis)

54
Q

What are the two effector mechanisms of Type IV Hypersensitivity?

A

(1) CD4+ T cells (TH1 or TH17) – helper cells produce cytokines that recruit macrophages which cause tissue inflammation that can lead to tissue injury (due to lysosomal enzymes, ROS and NO released from Macrophages)
(2) CD8+ CTLs – contribute to inflammation by killing host cells

55
Q

How long does it take for a type IV hypersensitivity reaction to devlop?

A

24-48 hours after Ag exposure

SFM Exam 2 (10 decks)

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