Lecture 32

Question 1

what is TIIIH mediated by?

name some examples?

Answer 1

IgG mediated via immune complexes

serum sickness and arthus reaction

Question 2

what causes TIIIH? how is it cleared? what causes the tissue damage?

Answer 2

immune complex deposition in tissues

phagocytosis
complment system

neutrophils

Question 3

how are the immune complexes formed?

Answer 3

union of antigen and antibody in circulation or tissues

Question 4

what is the mechanism of tissue injury?

Answer 4

persistent ICs in tissue activate the complement which release anaphylatoxins that stimulate basophils and mast cells which release histamine, this increases vascular permeability and deposition of immune complexes

neutrophils attracted to area with the ICs and release enzymes and ROS, increase tissue damage and inflammation

platelets aggregated with consequences, release histamine and micro thrombi leading to ischemia

Question 5

name the localized immune complex disorder deposited in a particular organ like the kidney and joints?

Answer 5

arthritis or arthus reaction (farmers lung)

Question 6

name the generalized or systemic complex disorder formed in circulation deposition in many organs

Answer 6

serum sickness

Question 7

clinical manifestations of TIIIH?

symptoms (acute)?

Answer 7

fibrinoid necrosis
vaculitis
arthritis
glomerulonephritis
fagv

fever
splenomegaly
nausea/vomiting
lymphadenopathy 
fsln

Question 8

large amounts of Ag entering the blood stream are local or generalized reactions?

Answer 8

generalized reactions TIIIH

Question 9

what are the types of serum sickness? is this general or local TIIIH response

Answer 9

acute and chronic

generalized

Question 10

If single large dose of antigen is given – it acts as primary dose
This is self-limiting – with rise of Ab production, complexes become larger and more susceptible to phagocytosis

what type of TIIIH is this and sickness?

Answer 10

acute TIIIH serum sickness

Question 11

If repeated or prolonged exposure to antigen, there is continuous antigenemia (e.g., SLE – persistent antibody response to auto-antigen)

what type of TIIIH is this and sickness?

Answer 11

chronic TIIIH serum sickness

Question 12

what mediates TIVH?

Answer 12

T cell mediated (TH1, TH2, CTL) delayed type hypersensitivity

contact dermatitis, tuberculin reaction

chronic asthma, allergies

graft rejection

Question 13

Type IV hypersenstivity also known as?

Answer 13

delayed type hypersensitivity or DTH

Question 14

how does the type IV H work?

Answer 14

so CD4+ helper t cells recognize MHC II and become TH1 helper cells that secrete IL2 and IFN gamma which activate cytotoxic T cells and macrophages taking many days (48 hours)

Question 15

tissue injury due to TIV hypersensitivity is caused by or a combination of?

Answer 15

cytokine mediated inflammation or direct killing

Question 16

TH1 cells released due to TIVH secrete? which activates what?

Answer 16

IL2 and IFN-gamma, activate and proliferate T cytotoxic lymphocytes to kill cells in targeted tissues via ganulysin, granzyme, perforin

Question 17

what are the phases of TIVH?

Answer 17

sensitization phase
challenge phase

First exposure to th antigen is sensitization phase; second and all other exposures to antigen is challenge phase, causing “induration” - detected 18 hours after challenge, max 24-48 hours

Question 18

what are the antigens that elicit TIVH reactions?

Answer 18

infectious agent
environmental antigens/chemical
autoantigens
transplanted organs

Question 19

how are TIVH reactions best characterized?

Answer 19

tuberculin reaction
granuloma reaction
contact dermatitis

Question 20

what are the four subtypes of type IV H?

Answer 20

a is macrophages; b is eosinophils; c is cytotoxic T cells and d is neutrophils