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Exam 2 > Hypersensitivty part 2 lecture 9 > Flashcards

Hypersensitivty part 2 lecture 9 Flashcards

1
Q

Type III hypersensitivity

A

involves immune complexes formed from antibody and soluble antigen complexes which deposit in tissue

complement activated

neutrophils attracted to the area

cause local damage

involves IgG or IgM antibodies that react with soluble antigens to form immune complexes that are deposited in tissues.

consequence: complement and Fc mediated inflammation which leads to tissue damage

type III reactions can be systemic or localized

immune complex deposition

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2
Q

mechanisms of type III reactions

A

complement and FC receptor mediated inflammation

site of deposition of immune complexes lead to complement and Fc receptor mediated recruitment and activation of inflammatory cells, vasculitis.

in addition platelet aggregation occurs and leads to microthrombus formation.

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3
Q

immune complexes as trigger for increasing vascular permeability

A

immune complexes act on basophils and platelets to produce vasoactive amine release

amines cause endothelial cell retraction and increase vascular permeability

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4
Q

deposition of immune complexes

A

kidneys, joins, and small vessels, heart, and skin

types of antigens: infectious agents, innocuous substances, self antigen, persistence of ag facilitates IC formation

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5
Q

what makes immune complexes deposit?

A

size: large immune complexes are cleared. Small immune complexes are formed that do not fix complement and do not get cleared in complement

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6
Q

other variables

A

charge of the immune

class of immune complex

antigen characteristics

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7
Q

disease assocations

A

associated with many human diseases.

serum sickness

drug reaction

prominent rheumatic disese: rheumatoid, lupus, post streptococcal GN, and polyarteritis nodosum

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8
Q

serum sickness

A

antigen antibody complexes rom in circulation and deposit in tissues

complement levels in serum derease due to activtion

eventually excess (free ) antibody limits formation of complexes.

SX: rash, fever, arthralgia or arthritis

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9
Q

type III vs type II

A

type III circulating immune complexes. Deposition in tissue. Lumpy and bumpy immunofluorescence pattern

type II: circulating antibody to tissue. Linear immunofluorscence pattern.

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10
Q

pathologic lesions

A

lesions occurs in vessels (vasculitis), kidneys (glomerulonephritis), joints (arthritis)

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11
Q

chronic immune complex disease

A

repeated antigen exposure

results in formation of immune complexes which deposit in many tissues, see in many tissues

see in many autoimmune diseases such as rheumatoid arthritis and systemic lupus erythematosus

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12
Q

drug reaction (serum sickness)

A

a type of serum sickness caused by hypersensitivity to an intravenous injection of drug

penicillin most commonly implicated although many drugs

caused by drug specific immune complexes

small drug molecules may serve as haptens that bind to serum proteins then develop antibody response either to the hapten or the hapten protein conjugate

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13
Q

rheumatoid arhtirits

A

autoimmune disease characterized by inflamed synovium

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14
Q

role of rheumatoid factor

A

IgM which has specificity for determinants on the Fc portion of ht patients own IgG

this IgM antibody is called rheumatoid factor and is deposited in joints

also has a type IV component

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15
Q

lupus

A

chronic inflammatory disease targeting mainly joints, kidneys, heart, skin and lung.

immunologic features: auto antibodies to multiple nuclear antigens including double stranded DNA.

Antigen/antibody complex damage tissues by activating complement and by engaging Fc receptors on immune cells expressing these receptor

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16
Q

Post strep glomeruloephrtis

A

associated with infection group A strep

immunogloic features: immune complexes deposit in the lipid bilayer of the glomerular basement membrane. ACtivation of the classical complement pathway leads to damage to basement membrane

abrupt onset of symptoms 1-4 weeks after infection leads to dark or smoky colored urine

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17
Q

Localized type III reaction: arthus reaction

A

skin reaction which shows classic finding of Type III reaction

antigen injected intradermally in the presence of preformed antibody

get area of tissue necrosis and caused by antibody excess. Results from immune complex deposition. tetnus and diptheria

18
Q

measurement of immune complexes

A

measure levels of complement

will be decreased with active deposition of immune complexes. Simple test. readily available. indirect measure.

19
Q

treatment of type III hypersensitivity

A

immunosuppression for reactions against self antigen

antigen avoidance

20
Q

type IV hypersensitivity: T cell mediated

A

describe all hypersensitivity reaction which took more than 12 hours to develop

Delayed type hypersensitivity

include classic DTH reaction and T cell mediated.
transferred by cells, not serum

21
Q

Type IV 2

A

reaction is initiated by antigen specific TH1 cells

activated t cells and macrophages are the major cellular mediators of these reactions

cytokines are very important in amplifying and continuing the response

CD8 t cells- mediate direct killing

22
Q

hallmarks of a type IV reactions

A

delay in time required for the reaction to develop to re exposure to antigen

the recruitment of macrophages as opposed to neutrophils

extensive tissue damage

association with cytokines

Important in killing viruses and tumor antigens: destroy target cells by CD8 cells

lysis of targets cells are specific and dependent on Class I HLA antigens.

23
Q

target antigens

A

innocuous environmental antigens- often seen in contact dermatitis

self antigens: associated with autoimmune disease

intracellular pathogens that are hard to clear: mycobacterium

24
Q

disease associations type IV

A

contact dermatitis
autoimmune diseases: multiple sclerosis, type I diabetes, rheumatoid arthritis

graph rejection

tumor immunity

25
Q

infectious diseases manifesting delyaed hypersensitivity

A

many due to infectious agents: mycobacteria, protozoa, and fungi

diseases: TB, leprosy, leishmaniasis, listeriosis, deep fungal infection, sarcoidosis, and parasitic infections

viral hepatitis

26
Q

contact hypersensitivity

A

allergen is placed in contact with the skin

area of crusting with erythema at the site of contact with the allergen

reaction is maximal at 48 hours

induced by haptens such as nickel and chromate

bind to normal skin proteins and ecome antigenic

commonly caused by rubber, poison oak and ivy.

27
Q

contact hypersensitivity 2

A

sensitizing substance is often a hapten that complexes with skin proteins (carrier)

target organ is skin

antigens: substances like nickel, poison ivy, drugs

28
Q

histologic features

A

langerhans’ cells are the principal antigen presenting cells

cytokines are crucial in mediating and continuing the reaction

29
Q

test for detecting type IV reactions Patch test

A

an in vivo test to assess person’s reactivity to contact antigens

sensitizing antigen is place on the skin and convered with dressing

examined 48-72 hours later

30
Q

testing for detecting type IV reactions DTH test

A

an in vivo test to assess immunologic memory for specific antigens

antigen injected intradermally

reaction peaks at 48 to 72 hours

positive reaction only means person has been sensitized

a nonreactive person is called anergic

31
Q

DTH tests

A

measure induration, not simply erythema

antigens: PPD (purified protein derivative from mycobacterium tuberculosis), candida, teatanus, diphtheria

positive DTH skin test only tells you that there are sensitized t cells present

gives you no information on whether the disease is active

32
Q

tuberculin type hypersensitivity

A

classic DTH response

occurs as an erythematous indurated lesion

maximal 48-72 hours after challenge with tuberculin antigen in a sensitized individual

antigen applied intradermally

33
Q

TB test from blood

A

several tests now available for testing for TB exposure on whole blood

test for release of interferon gamma after incubation with TB antigen

called interferon gamma release assays

2 are fda approved: Quantiferon - TB gold in tube test; T spot

34
Q

IFGA

A

does not differentiate past from present infection

just demonstrates the presence of sensitized t cells

need to coreelate with clinical presentation to determine if the disease is active

35
Q

what are advantages of IGRAs?

A

requires a single patient visit to conduct the test

results can be available within 24 hours

does not boost responses measured by subsequent tests

prior BCG (bacillus calmette-guerin) vaccination does not cause a false positive IGRA test result; this is seen with in vivo DHT PPD testing

36
Q

What are limitations of IGRAs?

A

samples must be processed within 8-30 hours after collection while white blood cells are still viable

eroros in collecting or transporting blood specimens or in running and interpreting the assay can decrease the accuracy of IGRAs

limited data on the use of IGRAs to predict who will progress to TB disease in the future

37
Q

Other things to consider

A

limited data on the use of IGRAs for children younger than 5 years, persons recetnly exposed to M. Tuberculosis, immunocompromised persons, serial testing

test may be expensive

38
Q

appearance of the three main injection initiated skin tests

A

Wheal and flare: raised with well defined edge; soft wheal ~15mins

arthus reaction: larger reaction site and less defined edges ~5-12 hours

DTH reaction: Red undurated lesiion peaks at 48 to 72 hours

39
Q

anergy

A

inability to react to common skin antigens

this is tested by performing DTH skin tests, using a panel of commonly encountered antigens

40
Q

disease associataed with anergy

A

congenital imunodeficiencies; secondary or acquired immunodeficiency such as AIDS

autoimmune diseases: rheumatoid arthritis

malignancies: hodgkin’s disease, lymphoma, chronic lymphocytic leukemia

sarcoidosis

infections: influenza, mumps, measles, tb, leprosy, and others

41
Q

treatment of type IV hypersensitivity

A

antigen avoidance

anti inflammatory drugs

immunosuppression for reactions against self antigens

Exam 2 (23 decks)

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