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Immunology Exam 3 > Lecture 21: Hypersensitivity Disorders > Flashcards

Lecture 21: Hypersensitivity Disorders Flashcards

1
Q

What is an exaggerated IR thats harmful to the organism itself?

A

Hypersensitivity (or allergy)

  • it produces collateral to body
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2
Q
  1. What type of effector mechanism corresponds defenses against extracellular pathogens?
    * which hypersensitivities would these include?
  2. What type of effector mechanism corresponds defenses against intracellular pathogens?
    * which hypersensitivities would these include?
A
  1. Ab-mediated
    * Type I, II, III
  2. Cell-mediated (CD4+, CD8+ and MΦ)
    * Type IV
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3
Q
  1. What type of hypersensitivity produces immediate rxns and are mediated by allergens and IgE Abs?
  2. What cell types do IgE Abs activate and what do they release?
  3. What term describes ppl w/ strong propensity to develop allergic rxns?
  4. Which Th cell and their cytokine are impt for IgE production?
A
  1. Immediate type I
  2. Mast cells and eosinophils –> release inflammatory mediators
  3. Atopic
  4. Th2 produce IL-4 –> switch isotype to IgE Abs

(also follicular Th cells help with this)

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4
Q

Type 1 Hypersensitivity:

  1. Describe the 1° Allergen encounter (priming)
  2. Describe the 2° allergen encounter
A
  1. Allergen injested/inhaled/skin contact –> APC activates T cells (Th2) —> allergen delivered to LN where BCR specific for those allergens activates B cell –> IgE enters circulation and is bound rapidly by FcRε (CD23) on mast cells in tissue
  2. Upon 2° exposure to same allergen immediately bound to IgE on the mast cell –> cross-linking causes mast cell degranulation releasing –> vasoactive amines, cytokines/chemokines, lipids –> 3 primary repsonses
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5
Q
  1. What are the hallmarks for Type 1 hypersensitivity?
  2. What causes dilation of small vessels, increaes vascular permeability, and sm. m contraction? (granule exocytosis prod)
  3. What causes local tissue damage? (granule exocytosis prod)
  4. What is a lipid mediator stimulates prolonged sm. m contraction?
  5. What is a lipid mediator that causes vascular dilation?
  6. What causes local inflammation? What phase is this?
A
  1. Acute rxns and inflammation (caused by mast cell mediators)
  2. Histamine
  3. Proteases
  4. Prostaglandins
  5. Leukotrienes
  6. Cytokines –> TNF and IL-1
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6
Q

Type 1 Hypersensitivity Synopsis:

  1. When would no clinical signs be seen?
  2. When does allergic dz result?
A
  1. Primary exposure
    * Allergen exposure –> Ag activaiton of Th2 cells –> stim of IgE class switching –> production of IgE –> binding of IgE to FcεR1 on mast cells
  2. Secondary exposure
  • repeat allergen exposure
  • allergens bind and cross-link memb-bound IgE –> Mast cell activaiton causes release of:
    • vasoactive amines –> IMMEDIATE rxn = w/in second to minutes
    • cytokines (TNF and IL-1) –> LATE PHASE rxn = w/in 6-24 hrs
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7
Q

What are the events in IMMEDIATE reaction vs Late-phase rxn in Type 1 hyerpsensitivity?

What are some examples of Type 1 hypersenstivity?

A
  1. Immediate: w/in minutes
  • immediate vascular and sm. m reaction to allergen
  • vasodilation, congestion, edema
  1. Late-phase: w/in 2-24 hrs
    * inflammatory infiltrate rich in eosinophils, neutrophils, and T cells
  2. Systemic anaphylaxis, acute urticaria, allergic rhinitis, asthma, food allergy
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8
Q
  1. What is a major example of a local type 1 hypersensitivity rxn that causes reversible airway obstruction due to release of inflammatory mediateors from mast cells upon allergen encounter?
  2. What occurs when an allergen causes systemic release of vasoactive amines from mast cells and a flood of cytokines after absorbed allergen is distributed thru body via circulation?
A
  1. Asthma
    * mediators cause loosening of tight jxns –> inc. cap permeability –> spasmatic contraciton of sm. m surrounding bronchi –> dec size of bronchial lumen –> SOB
  2. Anaphylaxis (systemic)
  • sm. m contraction, vasodilation cap endothelium
  • blood retention in tissues –> BP drom –> vascular shock
  • inc contraciton of sm. m surrounding bronchi –> breathing difficult
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9
Q
  1. What is a primary property that is unique to all allergens?
  2. What is the key mechanism of allergen-specific immunotherapy (SIT)?
  3. What are the 3 aims of allergen-SIT?
A
  1. Produce IR at very low []
  2. Generation of induced regulatory FOXP3+CD4+CD25+ Treg cells
  • Induce peripheral T cell tolerance
  • inc threshold for mast cell and basophil activaiton via allergens
  • dec. IgE-mediated histamine release
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10
Q
  1. What type of hypersensitivity is mediated by non-IgE Abs that bind cell surface and tissue Ags (SOLID Ag) causing inflammation in a complement-dependent manner?
  2. Which complement pathway is activated and what are the complement byproducts that recruit leukocytes and induce inflammation?
  3. Abs opsonize (via C3b) leading to phagocytosis of cells via what 2 receptors, corresponding to what 2 cells?
  4. What are the inflammatory mediators of these 2 cells types?
A
  1. Type II Hypersensitivity
    * IgG and IgM abs activate complement
  2. Classical pathway; C3a and C5a
  3. FcRγ –> on neutrophil and CR1 –> on macrogphage
  4. ROS and lysosomal enz –> damage adj tissues and cause inflammation

*** Ags are bound to cell or tissue surface*** (they are not soluble)

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11
Q

Type II Hypersenstivity also has an Ab-dependent cellular cytotoxicity (ADCC) mechanism that is mediated by what cell type?

A

NK cells

  • via FcγRIII –> low affinity
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12
Q

1. Autoimmune hemolytic anemia is an example of what type of hypersensitvity?

  1. When does hemolytic dz of newborn occur?
A
  1. Type II hypersensitivity
  • target Ag = erythrocyte memb prtns (Rh blood group Ags)
  • causes opsonization and phagocytosis of RBC
  1. When mom is Rh-neg and fetus is Rh-pos
  • mom makes anti-Rh Abs and complement from fetus
  • only affects subsequent pregnancies
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13
Q
  1. Grave’s dz and myasthenia gravis are what type of hypersensitivity?
  2. During their MOA is there cell tissue/injury?
  3. Which dz is where the abs stimulate TSH receptors even in the absence of TSH causing ______?
  4. Which dz is where Abs inhibit binding of Ach to Ach receptors?
A
  1. Type II
  2. No cell/tissue injury (abs are either blocking or activating the receptors)
  3. Grave’s dz; hyperthyroidism
    * anxiety/irritability, tremor hands/fingers, heat sensitivity
  4. Myasthenia gravis
    * m. weakness, drooping of 1 or both eyelids, impaired speaking
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14
Q

What type of hypersensitivity is seen when mismatched ABO blood transfusion rxn occurs?

A

Type II

ex) donated type A blood w/ type A Ags enters bloodstream of type B recipient

Anti-A abs in plasma of type B recipient bind to the donated type A RBCs

Bound anti-A Abs activate complement –> hemolysis and release of Hb

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15
Q

What are the 3 drugs cause in Drug-induced hemolytic anemia (DIIHA) via Type II hypersensitivity rxn?

A
  1. Penicillin –> directly binds RBC surface –> anti-drug Ab
  2. Quinidine –> autoAbs form immune complexes w/ drug –> these bind to RBC via CR1
  3. Methyldopa –> antidrug Abs cross reactis w/ Rh Ag
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16
Q
  1. What Type II hypersensitivity condition, is a rare autoimmune dz that involves both lungs and kidneys?
  2. Its characterized by the destruction of what type of collagen found in the basement memb of renal glomeruli and pulm. alveoli?
  3. It manifests rapidly as what 2 clinical manifestations? (1 for kidney, 1 for lung?
A
  1. Goodpasture’s Syndrome
  2. Type IV
  3. Glomerulonephritis and necrotizing hemorrhagic pneumonitis
17
Q

Rheumatic fever is classified as what type of hypersensitivity rxn?

A

Type II

  • target Ag = streptococall pyogenes cell wall Ag
  • ab cross reacts w/ myocardial Ag
  • Inflammation and MΦ activation
  • mycarditis and arthritis
18
Q
  1. What type of hypersensitvity is mediated by Ab-Ag immune complexes?
  2. Are the Ags soluble or bound to tissue?
  3. _____ Ab-Ag immune complexes are may be formed in the ____ then deposited in BVs and tissues (primarily _____ and _____).
  4. What is activated as a result of the deposition of Ag-Ab immune complexes? (ie what is the major mechanism of tissue damage?)
A
  1. Type III
  2. Soluble **** (major difference b/w type II and III)
  3. Soluble; circulation; lungs and kidneys
  4. Complement (large amounts and via CP) which causes the release of C3a and C5a
  • inflammatory cells (NEUTROPHILS, mast cells and basophils) release vasoactive amines
  • inflammation caused by activated immune ceels
19
Q
  1. What type of hypersensitivity is Systemic Lupus Erythematosus (SLE)
  2. What are the most frequent type of auto-Abs are found in SLE?
  3. What are the clinical manifestations of SLE, these are caused by what?
  4. Which Ab is involved?
  5. Environmental triggers (ie. viral infection or DNA damage via UV radiation) activate what? Contributing to the secretion of IFN-1 and other cytokines, supporting lymphocyte autoreactivity
A
  1. Type III
  2. Anti-DNA Abs (testing for anti-nuclear Abs = diagnositc test)
  3. Rashes, arthritis, glomerulonephritis, and vasculitis
    * due to formation of immune complexes
  4. IgG
  5. TLR 7/9
20
Q
  1. What type III hypersensitivity dz is a SYSTEMIC necrotizing vasculitis affecting medium-sized MUSCULAR arteries?
  2. What virus may be associated?
  3. What do the immune complexes form b/w?
  4. What clinical manifestation is often seen?
A
  1. Polyarteririts nodosa (PAN)
  2. Hep B virus
  3. HBV surface Ag and host IgG –> deposit in BVs –> vasculitis
    * Tissue injury mediated by complement activation and accumulation of inflammatory cells in tissue
  4. Aneurysms in weakened vessel –> risk for rupture and hemorrhage
21
Q
  1. What dz is assoc. w/ glomerular trapping of circulating immune complexes made of nephritogenic bacterial Ags and IgG?
  2. Activation of complement via what pathway?
  3. Activation of what cell releases oxidants, proteases, and pro-inflammatory cytokines?
A
  1. Acute Post-Streoptococcal Glomerulonephritis (APSGN)
  • this is primarily Type III Hypersensitivity
  • (type II can be involved if there are nephritogenic bacterial Ags are already planted in kidney tissue then IgG will come bind forming the immune complex)
  1. Classical
  2. Neutrophils
    * complement + inflammatory prod –> glomerular tissue damage
22
Q

Which type III hypersensitivity dz is systemic vs local?

  • serum sickness
  • arthus reaction
A

Serum sickness = SYSTEMIC

  • injection of anti-serum/anti-toxin into pt
  • Fc receptors on endothel. bind antitoxin (Ab) that has reacted w/ toxoid
  • additional antitoxin and toxoid bind forming larger complex
  • CP activated –> C5a, C3a released attracting macrophages and neutrophils
  • involves kidneys, lungs and skin (but spreads throughout circulation

Arthus rxn = LOCAL

  • subcut. admin of prtn Ag to previously immunized pt –> immune complexes form at site of Ag injection –> local vasculitis
23
Q
  1. Type IV hypersensitivity is mediated by what?
  2. Type IV hypersensitivity and tissue injury can also be caused by T cell responses to _____
  3. Tissue injury/inflammation induced by cytokines produced by what two types cells?
  4. OR by direct killing of host cells via _____.
A
  1. T - cell mediated
  2. Microbes –> Mycobacterium tuberculosis
  3. Th1 and Th17 (CD4+ = cytokine-mediated inflammation)
  4. CD8+ CTLs
24
Q
  1. Type IV hypersensitivity is also known as what?
    * what is the time frame of activation?
  2. Th1 recruits _____. Th17 recruits _____.
    * what products do these two cell types release resulting in tissue injury
  3. Many AUTOIMMUNE dz’s caused by intercation of autoreactive T cells with ______ leading to cytokine releae and inflammaiton.
A
  1. Delayed typed hypersensitivity (DTH)
  2. macrophages; neutrophils
  • MΦ release –> NO and pro-inflammatory cytokines (IL-1 and 6)
  • Neutrophils –> lysosomal enz, ROS
  1. self-Ags
25
Q
  1. What are the 3 primary autoimmune dz’s mediated by type IV hypersensitivity?
  2. What are 2 inflammatory dz’s w/ microbial component?
A
  1. MS, RA, and type 1 DM
  2. Crohn’s dz (IBD and ulcerative colitis)
    * due to abberant rxns to intestine microflora which has autoimmunity component

Tuberculosis (due to rxns w/ microbial Ags)

26
Q
  1. MS is a result of ____ type of autoimmunity causing dz affecting brain.
  2. What must occur during primary exposure for MS to develop?
  3. Excess glutamate causes what?
A
  1. Th1
  2. Damage to BBB
  3. demyelination of neurons (bc oligodendrocytes are extremely sensitive to inc. glutamate)
27
Q
  1. RA, an inflammatory dz of small and large joints is a result of what type of hypersensitivities?
  2. What are all the cells involved?
  3. RA patients have circulating ______ that reacts w/ Fc portion of IgG mlcls?
A
  1. Mixed –> Type III/IV hypersensitivity (but primarily Type IV bc Th1 and Th17 are major contributers)
  2. Th1, Th17, activated B cells, plasma cells –> IgG, and MΦ
  3. Rheumatoid factors (auto-Abs)

Lymphocytes, Abs and immune complexes enter joints –> inflammation of synovium assoc w/ destruciton cartilage and bone

28
Q
  1. Type 1 DM is what hypersensitivity?
  2. Local APCs present Ag via ____ MHC and secrete _____ activating Th1 cells and CD8 T cells which further stimulate what cytokine?
  3. CD4 and CD8 T cells act against β-cell autoAgs via what type of autoantibodies?
  4. These β-cell autoAgs would be classified as ____ bc they are hidden inside the β-cell.
A
  1. Type IV
  2. Class II; IL-12; IFN-γ
  3. Islet cell autoAbs
  4. cryptic

** once activated islet specific T cells traffic to pancrease where they proliferate and accumulate causing inflammation and destruction of β-cells

29
Q

Contact dermatitis with poison ivy is what type of hypersensitivty reaction?

A

Type IV –> DTH

  • Haptens (small pentadecacatechol mlcls) interact w/ skin proteins –> w/in 7-10 days T cells sensitized and T memory cells formed
    • this is primary contact –> no sx
  • secondary contact –> w/in 1-2 days T memory cells develop into many active T cells –> dermatitis
30
Q

DTH can be used to confirm dx.

  1. They are ____ - mediated inflammatory rxn resulting from activation of CD4+ T cells.
  2. How long does this rxn typically take to develop?
  3. Humans can be sensitized for DTH rxns by TB (microbial infection), Poison ivy (contact sensitization) or diptheria toxin/tetanus toxin (immunizaiton).
  4. Wht prtn Ag of mycobacterium tuberculosis elicits a DTH rxn called tuberuclin rxn?
A
  1. cytokine
  2. 24-48 hrs
  3. PPD = purified protein derivative

Immunology Exam 3 (6 decks)

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