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Immunology Final Exam > Hypersensitivity Reactions > Flashcards

Hypersensitivity Reactions Flashcards

1
Q

Hypersensitivity (Allergy) (3)

A
  • exaggerated and inappropriate reaction to an otherwise harmless antigen
  • immune system is reacting in a damaging rather than a protective fashion
  • may develop during humoral or cell-mediated immune responses
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2
Q

Immediate hypersensitivity reactions

A

-Hypersensitivity reactions involving antibody or antibody-antigen complexes (i.e., humoral) are characterized by symptoms that manifest within minutes or hours

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3
Q

Type I-IgE-mediated Hypersensitivity-First Exposure

A
  • On first exposure, Th2 response to allergen results in IgE production by plasma cells
  • IgE binds to high affinity Fcε receptors on the surface of eosinophils, basophils and mast cells, ‘sensitizing’ these cells.
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4
Q

Type I-IgE-mediated Hypersensitivity-Second Exposure

A

Second exposure to the allergen cross-links Fc(E)RI-bound IgE, causing degranulation and release of pharmacologically active mediators

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5
Q

Allergens

A
  • nonparasitic antigens that stimulate type I hypersensitivity reactions in allergic individuals
  • Most responses occur at mucous membranes
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6
Q

Atopy

A

A hereditary tendency in some individuals to make IgE in response to common environmental antigens

  • This results in tissue-damaging IgE-mediated hypersensitivity reactions
  • have high serum IgE and increased number of circulation eosinophils
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7
Q

Type 1 hypersensitivity-parasites

A

-believed to be related to clearance of parasites

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8
Q

Systemic anaphylaxis

A

a shock-like and often fatal type I hypersensitivity reaction

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9
Q

High affinity receptor for IgE (FcεRI)

A
  • consists of 4 polypeptide chains
  • The α chain interacts with IgE Fc region
  • the β chain links the α chain to the disulfide- linked gamma chain homodimer.
  • Each gamma and beta chain possesses an ITAM that interacts with TKs to transduce an activating signal
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10
Q

Low affinity receptor for IgE (FcεRII; CD23)

A
  • The FcεRII consists of a single type II polypeptide chain
  • involved in regulating IgE response and depends on interactions between IgE/CD23 and soluble CD23 binding to CD21 on the B cell.
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11
Q

Cell types expressing FCεR- Mast cells (4)

A
  • Large, granulated mononuclear cells derived from bone marrow precursors
  • Tissue mast cells are found in connective tissue near nerves and surrounding blood vessels
  • Mucosal mast cells are found in the mucosa lining the gut and lungs
  • Express high affinity receptors for the Fc portion of IgE
  • Synthesize and secrete allergic mediators, as well as a large number of cytokines.
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12
Q

Cell types expressing FCεR-Basophils

A
  • Circulating white blood cell that resembles mast cells
  • Recruited from the blood into inflamed tissue.
  • Granulated morphology with a multi-lobed nucleus; Express high affinity receptors for the Fc portion of IgE.
  • Synthesize and secrete allergic mediators
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13
Q

Sensitization Phase of IgE mediated hypersensitivity reactions

A
  • Following antigen presentation, Th2 cells make IL-4, IL-5 and IL-13, B cells switch to IgE
  • IgE binds to high affinity IgE Fc receptors on tissue mast cells and blood-borne basophils
  • IgE stable longer when bound to receptor
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14
Q

Sensitization Phase of IgE mediated hypersensitivity reactions-PCA

A
  • passive cutaneous anaphylaxis

- passive transfer of IgE-containing serum will sensitize skin mast cells

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15
Q

Activation Phase of IgE mediated hypersensitivity reactions

A

-Cross linking of at least two high affinity IgE Fc receptors (and bound IgE) triggers mast cell and basophil degranulation
Cross linking by
-multivalent allergen
-anti-IgE antibody
-anti-Fc receptor antibody
-aggregated IgE.
-non IgE activators of mast cells include C3a, C5a, cold, exercise, neuropeptides

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16
Q

Early Effector Phase of IgE mediated hypersensitivity reactions- Mediators

A

-effector phase mediated by primary and secondary mediators that are released by activated mast cells and basophils

17
Q

Effector Phase of IgE mediated hypersensitivity reactions-Primary Mediators (preformed) (5)

A
  • histamine
  • eosinophil chemotactic factor-attract to site of mast cell degranulation
  • neutrophil chemotactic factor
  • proteases (degrade blood vessel basement membrane, stimulate mucus secretion, generate complement split products)
  • stored in granules attached to matrix protein (heparin) by electrostatic attraction
18
Q

Effector Phase of IgE mediated hypersensitivity reactions-Primary Mediator Histamine

A
  • binds to H1-4 receptors
  • histamine interaction w/ H1 receptors causes intestinal and bronchial smooth muscle contraction, increased vascular permeability, increased mucus secretion by goblet cells
  • H2 receptors cause vasodilation, increases vascular permeability, stimulates exocrine glands, causes acid release in the stomach
  • H2 receptors on mast cells and basophils suppresses further degranulation, acting as negative feedback control mechanism
19
Q

Effector Phase of IgE mediated hypersensitivity reactions-Secondary Mediators

A
  • must be synthesized
  • leukotrienes
  • prostaglandins
  • bradykinin
  • cytokines
20
Q

leukotrienes

A
  • a set of peptides that cause prolonged smooth muscle constriction (bronchoconstriction) that is independent of H1 receptor engagement
  • Vascular permeability and mucus production are also increased by leukotrienes.
21
Q

Prostaglandins

A

-cause platelet aggregation, vasodilation, and bronchoconstriction

22
Q

Platelet Activating Factor (PAF)

A

-causes platelets to aggregate and degranulate, releasing additional histamine that causes bronchoconstriction and vasodilation

23
Q

Bradykinin

A

-increases vascular permeability and causes smooth muscle contraction

24
Q

Cytokines

A
  • IL-4
  • IL-5
  • IL-6
  • IL-13
  • TNF
25
Q

Late Effector Phase of IgE mediated hypersensitivity reactions

A
  • localized inflammatory reactions within 4-6 hours of the initial allergic response that may persist for 1-2 days
  • infiltration of neutrophils, eosinophils, basophils, macrophages, and Th2 cells, likely a response to cytokines released by activated mast cells
26
Q

Late Effector Phase of IgE mediated hypersensitivity reactions-Eosinophils

A
  • attracted by eosinophil chemotactic factor
  • activated by binding to antibody-coated allergen via FcR for IgE and IgG, releasing inflammatory mediators (such as Major Basic Protein: MBP) that cause tissue damage.
  • IL-3, IL-5, and GM-CSF secreted by activated mast cells promote eosinophil growth and differentiation.
27
Q

Late Effector Phase of IgE mediated hypersensitivity reactions-Neutrophils

A

neutrophils are also attracted to the site of degranulation by NCF and IL- 8 released at the site
-Neutrophils release their granule contents including lytic enzymes, platelet-activating factor, and leukotrienes

28
Q

Systemic Anaphylaxis

A
  • life-threatening impaired breathing due to airway swelling
  • Uterine cramps, involuntary urination and defecation additional symptoms
  • due to smooth muscle contraction
  • hives, edema may result from fluid leaking into tissue spaces
  • blood pressure may drop, leading to anaphylactic shock
29
Q

Localized anaphylaxis

A

reaction in a specific tissue or organ
-allergen into the skin, cutaneous anaphylaxis characterized by
erythema (redness, blood vessel dilation) and edema (swelling due to release of serum into tissue)
- peaks ~10-15 min of challenge with the allergen (wheal and flare reaction)
-allergic rhinitis (hay fever) and asthma
-In asthma patients, infiltrating eosinophils and neutrophils can cause significant tissue damage.

30
Q

RAST and RIST

A
  • measure serum IgE levels
  • radioimmunosorbent test
  • radioallergosorbent test
31
Q

Environmental Medical Treatment of type1 hypersensitivity

A

-avoid the allergen

32
Q

Pharmacologic Medical Treatment of type1 hypersensitivity

A
  • antihistamines
  • Leukotriene antagonists
  • cortisone
  • epinephrine
33
Q

Immunologic Medical Treatment of type1 hypersensitivity

A

Hyposensitization
- repeated subcutaneous injections of the
allergen to induce the production of circulating allergen-specific IgG, to remove the allergen before it can trigger IgE sensitized mast cells and basophils
-May also cause a shift to a Th1 response
-Humanized monoclonal anti-IgE Ab that bind only to free IgE, can lower serum IgE levels and prevent mast cell/basophil sensitization

Immunology Final Exam (5 decks)

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