slide1 n.
Download
Skip this Video
Loading SlideShow in 5 Seconds..
Ch. 15. Hypersensitivities (Allergies) Atopy - hereditary predisposition toward allergies Mechanism not clear- may map PowerPoint Presentation
Download Presentation
Ch. 15. Hypersensitivities (Allergies) Atopy - hereditary predisposition toward allergies Mechanism not clear- may map

Loading in 2 Seconds...

play fullscreen
1 / 36

Ch. 15. Hypersensitivities (Allergies) Atopy - hereditary predisposition toward allergies Mechanism not clear- may map - PowerPoint PPT Presentation


  • 131 Views
  • Uploaded on

Ch. 15. Hypersensitivities (Allergies) Atopy - hereditary predisposition toward allergies Mechanism not clear- may map to chromosomal region encoding many cytokines Tend to occur on mucous membranes- allergens either inhaled or ingested Immediate or delayed type hypersensitivity (DTH)

loader
I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
capcha
Download Presentation

PowerPoint Slideshow about 'Ch. 15. Hypersensitivities (Allergies) Atopy - hereditary predisposition toward allergies Mechanism not clear- may map' - Sophia


An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.


- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript
slide1

Ch. 15. Hypersensitivities (Allergies)

Atopy - hereditary predisposition toward allergies

Mechanism not clear- may map to chromosomal

region encoding many cytokines

Tend to occur on mucous membranes- allergens

either inhaled or ingested

Immediate or delayed type hypersensitivity (DTH)

Gell and Coombs classification – Types I-IV

Ch. 15

slide2

p. 372

Ch. 15

slide3

IgE-mediated Hypersensitivity (Type I)

IgE discovered by Ishizakas in 1960s-

normally very rare in serum

Larger molecule than IgG

Not stable in serum

Binds to IgE receptors on basophils and mast cells;

then is stable for several weeks

Ch. 15

slide4

p. 374

Ch. 15

slide5

p. 373

Ch. 15

slide6

What are mast cells and basophils?

Basophil- rare blood cell

Mast cells- found in connective tissue

Granules contain active mediators

Also secrete lots of cytokines: IL-1, IL-4, IL-5, IL-6,

GM-CSF, etc.

Also have high- and low-affinity receptors for IgE

Ch. 15

slide7

Events in an allergic reaction:

First exposure

B cells produce allergen-specific IgE Ab

Tail of IgE Ab reacts with Fc receptors on

mast cells, leaving Fab’s directed away

from the cell surface

Second exposure

Allergen enters body, cross-links IgE on

mast cell in mucous membranes, skin, and

triggers release of chemicals  symptoms

Ch. 15

slide8

p. 377

Ch. 15

slide9

p. 379

Ch. 15

slide10

Histamine release occurs within minutes

Binds to receptors on target cells

smooth muscles contract

eosinophils attracted

mucus secretion

platelet activation

blood vessel dilation

Blocked by various compounds: antihistamines,

epinephrine, corticosteroids

Ch. 15

slide11

p. 380

Ch. 15

slide12

Effects of type I reactions

Systemic anaphylaxis

Respiration becomes difficult

Blood pressure drops

Smooth muscles of bladder and GI tract

contract

Bronchoconstriction

Countered by epinephrine

relaxes smooth muscles

decreases vascular permeability

improves cardiac output

Ch. 15

slide13

Localized anaphylaxis

Allergic rhinitis (hay fever)- nasal mucosa

Asthma- lower respiratory tract

bronchoconstriction,

edema

mucus

inflammation

Ch. 15

slide14

p. 382

Ch. 15

slide15

Early response - histamine, leukotrienes,

prostaglandins

bronchoconstriction, vasodilation,

smooth muscle contraction

Late response - IL-4, TNF-, etc.

endothelial cell adhesion

Also leukocyte migration, leukocyte

activation factors

Neutrophils (also eosinophils) cause a lot of

tissue damage

Ch. 15

slide16

Food allergies

cells are sensitized in GI tract

if Ag is blood-borne, can cause symptoms

such as asthma or hives

Atopic dermatitis (eczema)

Late-phase reactions (not asthmatic)

mast cells release cytokines

eosinophils, neutrophils recruited

Ch. 15

slide17

Regulation of type 1 hypersensitivity:

Antigen stimulation

IL-4 induced class switch

TH2 cells, also mast cells

IFN- reduces IgE production

Ch. 15

slide18

Detection of type I hypersensitivity (pp. 386-7):

Skin test

RIST- total serum IgE

RAST- IgE specific for a single allergen

Ch. 15

slide19

p. 386

Ch. 15

slide20

p. 387

Ch. 15

slide22

Therapies

Avoidance of Ag

Hyposensitization

Drugs

antihistamines (block receptors)

epinephrine (maintain high cAMP and

prevent degranulation

cromolyn sodium block calcium flux

and more (p. 388)

Ch. 15

slide23

Type II: antibody-mediated cytotoxic reactions:

Antibodies bind to cells and mediate their

destruction

Transfusion reactions (ABO blood group Ags)

Drug-induced hemolytic anemia

drugs absorb to RBCs, like hapten-carrier

Hemolytic disease of the newborn

Ch. 15

slide24
Ch. 15

p. 389

slide25

p. 389

Ch. 15

slide26
Ch. 15

p. 390

slide27
Ch. 15

p. 391

slide28

Type III: Immune complex disease:

Sometimes antibody- (soluble) antigen complexes

are not cleared like they should be

When deposited in tissue, they cause damage

complement activation- produces

inflammatory mediators

neutrophils are attracted

Arthus reaction - sensitized person develops

a reaction at site of exposure (slower than

type I)

Ch. 15

slide29

p. 392

Ch. 15

slide30

Generalized reaction- large amounts of antigen

enter bloodstream

Immune complexes form

Serum sickness- immunization with foreign serum

Complexes tend to accumulate in kidneys,

arteries, joints

Autoimmune disease

Infectious disease (malaria, parasitic disease)

Cross-reactivity with bacterial or viral antigens

Ch. 15

slide31

Type IV (TDTH and TC, or delayed-type):

Detected with skin test (e.g., tuberculin or PPD

skin test for tuberculosis)

Contact dermatitis- when small molecules

complex with skin proteins (poison ivy,

poison oak, cheap jewelery)

Internalized and presented by Langerhans

cells; TH1 response; influx of macrophages

Can lead to granuloma formation

Ch. 15

slide32

p. 394

Ch. 15

slide34

p. 397

Ch. 15

slide35

Helps protect against intracellular pathogens

Granulomas form in chronic reactions

DTH response declines in immunodeficient

people (with T cell deficiency), like AIDS

Ch. 15

slide36

p. 395

Ch. 15