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Immunology > Hypersensitivities > Flashcards

Hypersensitivities Flashcards

1
Q

Define hypersensitivity

A
  • any undesired immune response

- can be to an environmental object like allergies, or to self antigens and cause autoimmunity

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2
Q

State the four types of hypersensitivity and their major differences.

A
  1. Type I (immediate): typical allergic reaction; mediated by pre-formed IgE antibodies
  2. Type II (Cytotoxic-cell-bound antibody): antibody binding to target cells alters function via dealth, activate, inhibit; IgG or IgM
  3. Type III (soluble antibody immune complexes): antibody/antigen complexes float around and activate immune system; IgG or IgM
  4. Type IV (cell-mediated): T-cell mediated response
    * *1-3: end effect is antibody mediated (still involved T cell for antibody class-switching)
    4: end effect is T-cell mediated
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3
Q

Major difference between type II and type III hypersensitivity

A

-type II is antibody mediated but binds to cells and type III is also antibody mediated but binds to soluble proteins

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4
Q

Describe the primary response of Type I hypersensitivity

A

-there is not one on the primary exposure, however, the second exposure is immediate when the antigen is encountered

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5
Q

What is the effector molecule of Type I hypersensitivity?

A

-IgE antibody

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6
Q

When functioning appropriately, IgE does what? What about when it is directed against an inert substance?

A
  • -protect against parasites

- allergies

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7
Q

What is the name of the IgE receptor and what cells are activated by this receptor?

A
  • FcERI

- mast cells and basophils (when antigen cross-links the IgE)

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8
Q

What are the major effectors in the allergic response?

A
  • mast cells and basophils

- classical allergies is a type I hypersensitivity, so associate these cells types!

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9
Q

Compare and contrast mast cells and basophils

A
  • Both are large granule-contains cells full of active compounds (preformed inflammatory mediators)
  • both are sentinels of the immune system and let other immune cells know of the invader
  • both found in strategic locations of the host/environment interface
  • Mast cells are tissue resident cells that do not circulate, while basophils circulate and enter tissues
  • come from different lineages
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10
Q

T/F: Most of the body’s IgE can be found circulating in the blood.

A
  • false

- it is bound to the high affinity FcERI expressed exclusively on mast cells and basophils

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11
Q

3 properties of FcERI

A
  1. high affinity IgE binding receptor
  2. Binds monomeric IgE
  3. Expressed exclusively on mast cells and basophils
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12
Q

What is needed for mast cell and basophil degranulation? What is often released in the granules?

A
  • antigen needs to cross link RcERI to trigger cascade of events that lead to inflammatory mediator release
  • Histamine, serotonin, Eicosanoids/chemokines, cytokines
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13
Q

How many phases are there to the immediate (type I) hypersensitivity response? Name them

A

-2: acute and delayed

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14
Q

What happens during the acute phase of immediate hypersensitivity of the SKIN? What granule contents are released and that are their purposes?

A
  • degranulation of prestored contents by mast cells within seconds to minutes
  • one purpose is to recruit immune cells (eosinophils, basophils, neutrophils, T cells) to site of antigen encounter and allow them access
  • Histamine: vasodilation, increased vascular permeability (allows cells to enter site)
  • TNFa: activate endothelial cells to upregulate adhesion molecules
  • Proteases: destroy extracellular matrix to create pathways
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15
Q

What are the symptoms of the acute phase of immediate hypersensitivity of the skin and what causes them?

A

Wheal and Flare reaction: bump in middle (edema) with flare in perimeter (vasodilation)

  • itching: histamine
  • Swelling: edema
  • redness: vasodilation
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16
Q

Describe the purpose of the acute phase of immediate hypersensitivity in places other than the skin, like lungs, gut, and systemic circulation. Be sure to mention the purpose and major effectors and their functions.

A
  • purpose is to block pathogens from entering or to expel pathogens
  • Vasoactive amines (Histamine, serotonin) will increase secretion of mucus (mucosal linings), constrict visceral smooth muscle (bronchial and gut), and systemic vasodilation (shock-decreased BP)
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17
Q

What are the symptoms of the acute phase of immediate hypersensitivity in places other than the skin?

A
  • sneezing (itchy nose/throat)
  • coughing
  • chest tightness (difficulty breathing)
  • Diarrhea, vomiting (due to increased SM contractions)
  • Shock (decreased BP)
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18
Q

What is the worst case scenario in the acute phase of immediate hypersensitivity?

A

-anaphylaxis leading to respiratory blockage and shock

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19
Q

Describe what occurs in the late phase of immediate hypersensitivity.

A

-involves de novo production of mediators by mast cells/basophils, which takes a bit more time than degranulations (minutes to hours)

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20
Q

What are the 3 categories of mediators produced in the late phase of hypersensitivity and their actions?

A
  1. Eicosanoids (leujotrienes, prostaglandins): leukotrienes action is similar to histamine but much more potent; smooth muscle contraction, chemoattractant, increased secretions
  2. Chemokines (CCL3, MCP-1): attract e-phils, b-phils, n-phils, monocytes, T-cells
  3. Cytokines (IL-4, IL-6, TNFa): immine cell activation and Th2 polarization
21
Q

Acute vs. Late phases of immediate hypersensitivity

A
  • Mast cells: acute involves prestored mediator release; late involves de novo synthesis of inflammatory mediators
  • Acute: creating pathway for immune cell entry
  • Late: active recruitment of inflammatory cells
22
Q

Allergic symptoms depend on what 2 things?

A
  • route of entry and degree of systemic spread

- antigen entering the blood could result in anaphylaxis

23
Q

4 categories of treatment for Type I hypersensitivity

A
  1. blocking mediators
  2. reversing symptoms
  3. blocking mast cell degranulation and inflammation
  4. blocking IgE
24
Q

2 mechanisms to block mediators in treating type I hypersensitivity

A
  1. anti-histamines (mild allergies)

2. Leukotriene antagonists (asthma)

25
Q

3 mechanism to reverse symptoms in treating type I hypersensitivity

A
  1. Epinephrine (increase BP, block degranulation, anaphylaxis)
  2. Beta agonists (relax bronchial constriction; asthma)
  3. Anticholinergic (relax bronchial constriction and reduce mucus; asthma)
26
Q

2 mechanisms to block mast cell degranulation and inflammation in treating type I hypersensitivity

A
  1. Cromolyn sodium (mast cell stabilizer; mild allergies)

2. Corticosteroids (blocks degranulation and reduces inflammation; asthma)

27
Q

2 mechanisms to block IgE in treating type I hypersensitivity

A
  1. antigen desensitization (builds tolerance to antigen; chronic allergies; atopy)
  2. Anti-IgE antibody (block binding of IgE to R on cells; chronic allergies; atopy)
28
Q

Define an atopic individual and explain the causes.

A
  • an individual genetically or environmentally predisposed to developing type I hypersensitivity
  • Genetic: genes that predispose to IgE production (Th2 T cells)
  • Environmental: hygiene hypothesis (gut flora influences Th2 predisposition by unclear mechanisms but thought that an absence of diversity lead to hyper Th2 expression)
29
Q

Characteristics of allergens

A
  • most antigens are not allergens
  • need to get in to the right places and be stable at low doses
  • mimic parasite proteases whose activity mimics parasites and thus are attacked
  • *proteins** bc need T cell response
30
Q

What is type II hypersensitivity mediated by and what is it directed against?

A
  • mediated by CELL-bound antibodies (mainly IgG but also IgM)
  • directed against foreign antigens like drugs and transfused RBCs
  • Directed against self-antigens like self RBCs/platelets, activate receptors, block receptors
31
Q

What are the 2 main types of type II hypersensitivity?

A
  • cytotoxic

- receptor blocking/stimulating

32
Q

What are the 3 mechanisms involved in cytotoxic-type type II hypersensitivity?

A
  1. opsonization (IgG+ complement) clearance by phagocytes
  2. Antibody-dependent cell cytotoxicity (ADCC): NK cells express FcGRIII and will kill IgG-coated cell
  3. Complement-mediated lysis (mainly IgM, but sometimes IgG): MAC complex formation on cells will kill target cell
33
Q

Give the mechanism of receptor blocking/stimulating type type II hypersensitivity? Does this ever go by another name? Give 2 examples of this clinically.

A
  • Antibody binds to specific receptor on cell and block or stimulate function as opposed to inducing clearance of the cell
  • also known as type V hypersensitivity
  • Grave’s Disease: antibody stimulates receptor without hormone leading to hyperthyroidism
  • Myasthenia Gravis: antibody inhibits AChR in NMJ leading to early exhaustion of muscle under repetitive movement
34
Q

What mediates type III hypersensitivity and what is it directed against?

A
  • antibody/antigen complexes (IgG) that form immune complexes that deposit into tissues, causing inflammation by activating complement and FcGRIII on immune cells
  • directed against foreign antigens (soluble foreign proteins or pathogen-derived proteins) or self antigens (nuclear antigens in SLE or Neutrophil antigens in Wegener’s vasculitis)
35
Q

Effector mechanisms of type III hypersensitivity

A

Immune complexes are deposited in tissues and blood vessels

  • these IgG immune complexes activate Fc gamma R and complement. 1) Complement components act as chemoattractants and recruit neutrophils
  • 2) activation of R causes cytokines, enzyme, chemokine, and ROS release from immune cells
36
Q

What cells express FcGRIII?

A

-neutrophils, mast cells, monocytes, and NK cells

37
Q

When will immune complexes form in type III hypersensitivity?

A
  • at the zone of equivalence: when antigen and antibodies are in similar amounts when the immune system revs up
  • early during the infection, antigen»> antibody and little complex forms; at the end of the infection, antibody»»antigen and little complex forms (Zone of antigen excess, Zone of antibody excess)
38
Q

Immune complexes can be formed with antigens from pathogen and antibody to clear the pathogen. Give 3 places and clinical examples of where these IgG immune complexes could deposit in.

A
  1. blood vessels: vasculitis (Hepatitis C)
  2. Joints: reactive arthritis (bacterial strains)
  3. Kidneys: glomerulonephritis (GAS)
39
Q

Give 2 clinical examples of when immune complexes form against self antigens.

A
  1. Systemic Lupus Erythematosus: immune complexes formed with nuclear antigens and DNA; 4/11 critera to diagnose (serological, lab, clinical); symptoms vary based on organ affected, which is commonly kidney, joints, lungs
  2. Wegener’s Granulomatosis: immune complexes formed against neutrophil antigens like proteinase-3; symptoms related to blood vessel damage (vasculitis) and commonly affects nose, kidney, lungs, joints
40
Q

What is another name for Type IV hypersensitivity? What is it mediated by? What is it directed against?

A
  • delayed type hypersensitivity (DTH)
  • mediated by CD4+ and/or CD8+
  • antigen activates antigen-specific T cells and mounts an exaggerated response on reintroduction or chronic exposure of antigen
  • directed against foreign antigens (environment or pathogen) or self (MS or Hashimoto’s thyroiditis)
41
Q

2 effector mechanisms of Type IV hypersensitivity. What is the end result?

A
  1. inflammation by cytokine/chemokine release from CD4+ T cells
  2. Direct killing of cells by CD8+ T cells (cytotoxic T lymphocytes; CTLs)
    * *End result to both is tissue injury
42
Q

Mechanism of Type IV Hypersensitivity directed against foreign antigens and give examples.

A
  • first contact sensitizes person and subsequent contacts elicit a reaction
  • reactions are delayed by one or more days (DTH) due to migration of macrophages and T cells to site of foreign antigens
  • reactions frequently displayed on skin: itching, redness, swelling, pain
  • TB skin test, poison ivy, metals, latex gloves
43
Q

If poison ivy’s chemical urushiol is just a hapten, how does it generate T cell responses?

A

-it binds to or alters MHC peptide in a way that overactivates TCRs

44
Q

2 examples of when T cells via Type IV hypersensitivity act against self antigens

A
  1. Multiple sclerosis: T cells specific to proteins from oligodendrocytes; CNS inflammation with demyelination = slow nerve conduction velocity; commonly affects vision, motor function, sensation
  2. Hashimoto’s Thyroiditis: T cells specific to thyroglobulin; destroy thyroid hormone-producing cells in thyroid gland; common cause of hypothyroidism
45
Q

What is one way to block progression of MS?

A

-Natalizumab: antibody that blocks alpha4 integrin that effectively will block entry of T cells into brain

46
Q

GVHD is an example of what type of hypersensitivity?

A

-Type IV

47
Q

What occurs in GVHD?

A

-a fraction of donor T cells react strongly with recipient MHC (by chance ~2-5% will recognize allo-MHC) since donor T cells were not negatively selected by recipient MHC

48
Q

Bone marrow transplantation GVHD vs. Transfusion-associated GVHD

A
  • BM: donor T cells will attack all host tissues causing GVHD; commonly affects skin, GI tract, lung and liver inflammation; high morbidity which is barrier to HSCT (hematopoietic stem cell transplantation
  • TA: occurs mainly in immunosuppressed individuals; almost always fatal from bone marrow failure, since bone marrow is a target in TA-GVHD**MORE FATAL THAN BM TRANSPLANT*

Immunology (13 decks)

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