in response to allergies/anaphylaxis (hay-fever, asthma) - Th2 produces IgE and histamine from mast cells (high IL-5) - later reaction is mediated by leukotrienes, PGD2 - symptoms: vascular dilation, sm. m. contraction, mucus production

Mechanisms of Immune Injury Flashcards by Nick Jobeun

What antigens attract women to men?

HLA

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Haptens

molecules that bind to bodily proteins and becomes attacked by immune system
- cause of small molecule allergies (nickel, poison ivy)

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What does adaptive immunity consist of?

B/T-lymphocytes

-specific and diverse receptors for antigens

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Function of B-Lymphocytes

neutralization of microbe, phagocytosis, complement activation

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Function of Helper T-lymphocytes (CD4)

Activation of macrophages, inflammation, activation/profileration of T/B lymphocytes

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Function of cytotoxic T lymphocytes (CD8)

killing infected cells

- acute cellular rejection

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Function of Regulatory T-lymphocytes

suppression of immune system

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Function of NK cells

killing infected cells

- cells with no MHC I expression

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What cytokine lines the medulla of the lymph node?

Dendritic Macrophages

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What cytokines process antigens in outer skin?

Dendritic cells

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What cytokines are produced to by Th1? To defend against what?

IFN-gamma for intracellular microbes

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What cytokines are produced to by Th2? To defend against what?

IL-4, IL-5, IL-13 for helminthic parasites

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What cytokines are produced to by Th17? To defend against what?

IL-17, IL-22 for extracellular bacteria, fungi

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Where doe B-cells undergo maturation?

germinal follicles of lymph nodes

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Where are plasma cells generally found?

Produce antibodies in tissue rather than blood

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Hypersensitivity

disease caused by the immune system causing harm to the body

- failure of control through feedback mechanisms

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Type 1 Immune Injury

in response to allergies/anaphylaxis (hay-fever, asthma)

Th2 produces IgE and histamine from mast cells (high IL-5)
later reaction is mediated by leukotrienes, PGD2
symptoms: vascular dilation, sm. m. contraction, mucus production

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What is a common cause for urticaria?

IgE/Type I immune injury

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What is a common cause of eosinophilic gastroenteritis?

food allergy

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Cause of anaphylaxis

massive IgE-mediated response

Cause of atopic dermatitis

people with allergies

- look for FCeRI and dendritic macrophages

What is chronic urticaria and it’s cause?

patches of skin that swell from local IgE/histamine

- from autoimmunity, food, “unknown”

Cold urticaria

get hives from cold temperatures

- non-immune mediated

Cholinergic urticaria

hives from wet heat (sweating, shower)

- non-immune mediated

Dermatographism

skin gets inflamed where it is scratched

Type II Immune Injury

antibody mediated - antibodies attack antigen (autoimmune hemolytic anemia, goodpasture syndrome) - IgG, IgM

Coomb's test

test for antibodies in patient's blood

Goodpasture's disease

antibodies against basement membrane of lungs and kidney

Why are men preferentially used as plasma donors?

Women can have antibodies in the plasma against HLA antigens from previous pregnancy

What is the most common cause of hypothyroidism?

Autoimmunity (hashimoto's thyroiditis) | - antibodies and T/B-cells

Type II immune response in adrenal

Addison's disease | - T-cell destruction

Type II immune response in pancreas

Type I Diabetes Mellitus | - t-cells destroy islet of langerhans

What clotting factor do hemophiliacs develop antibodies against?

Factor VIII

What receptors do antibodies in Graves' disease bind to?

TSH receptors causing hyperthyroidism

Isaac's antibodies

Ab against muscles | - keeps muscles firing and causes pain

Type III immune injury

immune complex-mediated (vasculitis, arthritis, glomerulonephritis) - Ag + Ab + Complement - deposits into vascular intima (feel bad all over) - ends when antibody becomes more abundant and immune complexes leave

What type of immune injury is associated with fibrinoid necrosis ?

Type III

Arthus Reaction

sore muscles from injection of something that you already have Ab for

What type of immune injury is associated with hyperacute rejection of donor kidney?

Type III

Type IV immune injury

T-cell mediated (contact dermatitis, MS, rheumatoid arthritis, psoriasis) - inflammation --> cytolysis - Th1/Th17

Anergy

no immune response to things you have already encountered - dysfunction in T-helper cells (sarcoidosis, lymphomas, cancers, HIV, measles)

Halo nevus

T-cells destroy melanocytes around nevus

What cells are responsible for granuloma formation?

Th1 (no Ab necessary) | - miliary TB

What is responsible for acute humoral rejection?

antibodies | - intimal hyperplasia in arteries

Hyperacute rejection

Type III response - IgG precipitates - fibrinoid in arterial walls (lymphocytes)

What is responsible for acute cellular rejection?

CD8 - destroy heart transplant - tubulitis, endotheliitis

Chronic transplant rejection

vessels narrow or totalled - intima is thickened (concentric) - T-cells cause thickening of intima/media

Signs of acute graft v host disease

days to weeks after transplant - attack by CD8, Type IV immune response - generalized rash, loss of epidermis (starts in palms) - jaundice from bile duct damage - ulcers along GI tract/orally

Signs of chronic graft v. host disease

appears after ~100 days - more fibrosis, less necrosis - fibrosis of dermis with loss of skin - cholestatic jaundice from bile duct damage - GI damage - damage of host T-cells (immunocompromised) - cytomegalovirus pneumonitis infection