Lecture 31 - Autoimmunity, Hypersensitivity and Skin I

Question 1

Immune hypersensitivity - type I?

Answer 1

IgE mediated allergic reaction or anaphylaxis

Question 2

Immune hypersensitivity - type II?

Answer 2

IgG antibody-mediated (cytotoxic)

Question 3

Immune hypersensitivity - type III??

Answer 3

IgG immune complex regulated

Question 4

Immune hypersensitivity - type IV?

Answer 4

T cell mediated (DHT - delayed type)

Question 5

Mast cell degranulation?

Answer 5

antigen cross links IgE on mast cells (also triggered by C3a, C5a and some drugs) which causes release of mediators - chemoattractants, activators and spasmogens

Question 6

Allergies & causes?

Answer 6

rhinitis (dust mites, animal hair, pollen), insect stings (proteins in venom), food allergies (wheat and milk proteins, peanuts), small molecules (penicillin, morphine, codeine)

Question 7

Allergy treatments?

Answer 7

avoidance, antihistamines, corticosteroids, sodium cromoglycate (stabilises mast cells), epinephrine (for anaphylaxis), desenstisation (introduce IgG reaction to compete with IgE)

Question 8

Type II Hypersensitivity - physiology & e.g.?

Answer 8

antibodies against cell surface antigens, causign ADCC, complement activation, and frustrated phagocytosis e.g. organ specific autoimmunity and haemolytic disease of the newborn

Question 9

Type III hypersensitivity - physiology?

Answer 9

antibody response to circulating antigen (chronic disease), antibodies appear as antigen circulation becomes high -> immune complex-induced vasculitis and nephritis

Question 10

Type III hypersensitivity - blood vessel effect?

Answer 10

platelet aggregation -> microthrombus formation -> complement activation of neutrophil -> chemotaxis -> vascular damage

Question 11

Type IV hypersensitivity e.g.?

Answer 11

Mantoux test - immune (T cell) memory assessment; contact sensitivity - antigen (aka. hapten) uptake, processing and presentation to memory Th1 cells -> cytokine mediated Th1 cytokine-mediated inflammation (lymphocytes and macrophages)

Question 12

Autoantibodies?

Answer 12

natural IgM low affinity; Anti-nuclear antibodies seen in patients w SLE and in elderly; Anti-thyroid antibody seen in thyroid disease and elderly;

Question 13

Mechanisms of tolerance?

Answer 13

clonal depletion (central - BM and thymus), clonal regulation (peripheral - no co-simulation, anergy), suppression (peripheral - tregs control self-reactive cells) and ignorance (privileged sites and sequestered antigens)

Question 14

Molecular mimicry?

Answer 14

HLA presents self-antigen similar to bacterial, T cell thinks they look the same (not are), HLA haplotype dependent

Question 15

Goodpastures syndrome?

Answer 15

antibodies against type IV collagen in glomerular basement membrane

Question 16

MG?

Answer 16

antibodies block Ach receptors

Question 17

Hashimoto’s thyroiditis?

Answer 17

antibodies and T cells destroy thyroid tissue

Question 18

ITP?

Answer 18

idiopathic thrombocytopenic purpura - antibodies against platelets

Question 19

Addison’s disease?

Answer 19

destruction of adrenal cortex, hyperpigmentation

Question 20

Type 1 diabetes?

Answer 20

CD8 T killer cells attacking beta cels of islet of langerhans

Question 21

Pernicious anaemia?

Answer 21

antibodies against B12 or intrinsic factor preventing B12 absorption

Question 22

Grave’s disease?

Answer 22

Anti-TSH receptor autoantibody over-activates TSH receptor increasing Thyroxin release -> chronic thyroid stimulation by autoantibody

Question 23

Systemic autoimmune disease (type III) e.g.?

Answer 23

systemic lupus erythematosus (w butterfly rash) and RA

Question 24

Genetic predisposition?

Answer 24

antigen receptor genes (immunoglobulin and TCR), antigen presenting genes (associations w class I and II), complement genes (impaired immune complex clearance), regulatory genes (cytokines and co-stimulators)

Question 25

Treatment?

Answer 25

either replacements (insulin, thyroxin, -corticoid replacement) or suppression (immunosuppresives e.g. corticosteroids)