Allergic response and autoimmune Flashcards by Ethan Nieuwenhout

Type 1 hypersensitivity

Anaphylactic, due to inhaled particulate, IgE on granulocyte cells (mast cells, eosinophils)

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Mast cell soup

Enzymes for tissue remodelling, histamine and heparin (usually to fight parasites). TNF-alpha

Produced after, lots of IL, chemokine (CCL3), leukotrienes, platelet activation factor

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IL-4 and 13

Mast cell
Stimulate and amplify Th2 response, IL-4 is key for selecting IgE production in b-cells

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IL-3 and 5

Mast cell and eosinophil
promote eosinophil production and activation (type 1 response)

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CCL3

mast cell
chemokine for leukocytes

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Leukotrienes

smooth muscle contraction, vascular permeability, mucus production

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Platelet activating factor

chemotactic, increases lipid mediators

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Arachidonic acid

membrane fatty acid converted to leukotrienes or prostaglandins

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Mast cell effect on GI

increased fluid secretion and peristalsis to move things out

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Mast cell effect on airways

inflammation and increase mucus secretion

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Mast cell effect on BV

increased blood flow and permeability, increased lymph flow and inflammation

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Eosinophil location

underlying epithelial/ mucosal surfaces (respiratory, GI, urogenital tract), very little in blood

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Eosinophil soup

immediate
Peroxidase (kills and triggers histamine from mast cells),collagenase,major basic protein (toxic releases histamine), eosinophilcationic protein (neurotoxin)
Produced
IL 3 and 5 (increase eosinophil production in bone marrow), CXCL8 chemokine, leukotrienes, platelet activating factor

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Eosinophil peroxidase

Eosinophil
toxic via halogenation, also triggers release of histamine from mast cells

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Eosinophil collagenase

remodels connective matrix

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major basic protein

eosinophil
toxic to parasites and our cells, also triggers histamine release from mast cells

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eosiznophilcationic protein

toxic to parasites and neurotoxin

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Basophil granules

IL-4 and IL-13 for Th2 activation

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GI type 1 reaction

activated mast cells degranulate into BV causing wide spread urticaria, SMC issues, vomiting and diarrhea

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Pharmacological Tx

-Block pathways (histamine antagonist)
-suppress leukocytes (steroids)
-Prevent degranulation (cromolyn)
-constrict BV and SMC (epinephrine)

IgE desensitization

Shift towards IgG4, series of Ag injections gradually increased

Type 2 hypersensitivity

cytotoxic
small molecules covalently bound to human cells, forms an Ag looking structure which IgG attaches to and activates.
E.G penicillin

Type 3 hypersensitivity

Immune complex
forms small insoluble complexes of Ag and Aby that deposit on BV, kidneys or lungs and activate complement causing
Happens when there is too little Aby and complement does not clear it in the infected tissue
inflammation

Type 3 hypersensitivity cause

can happen when inj. with a Aby from another species (serum sickness) within 4-10 days
fever, arthralgia, GI upset, decrease complement conc, lymphadenopathy

Type 3 rash

Forms polycyclic wheal swelling, over lap but have clear dot in the middle. everywhere, oral oedema without mucus

type 3 arthus Rx

local erythema and hard induration (can't pop) after SC Ag injection (tetanus, diphtheria)

Farmers lung

type 3 reaction from inhaled Ag depositing complexes in lungs

Type 2 and 3 treatment

Discontinue mild: antihistamines anaphylaxis: epinephrine, O2, Airway, ECG monitor

Type 4 hypersensitivity

Delayed type or contact type Ag and T-cells mostly Th1 from sting or bite, CD8 t-cells from lipid small molecules (plant toxins), also immune rejection

Delayed type reaction

proteins from insects or bacteria erythema, induration, dermatitis, edema

Contact type reaction

from haptens (small toxins) or metals erythema, edema, dermatitis

Type 4 treatment

avoid contact, monitor for infection from scratching, steroids, cyclosporine, immunotherapy

Autoimmune start

begins with one of the hypersensitivity types (2,3 or 4) nothing has been linked with IgE

Autoimmune Type 2

usually target RBC, IgG and IgM are targeting RBC Ag and activating complement (MAC, opsonization C3b, spleen)

Subacute bacterial endocarditis

Type 3 complexes with bacterial Ag confused for self Ag causing renal failure

Mixed essential cryoglobuliemia

type 3 complexes with Rheumatoid factor causing vasculitis

systemic lupus erythematosus

Type 3 complexes with DNA, histones, ribosomes causing renal failure, vasculitis or arthritis

type 1 diabetes

type 4 T-cells target beta cells

rheumatoid arthritis

type 4 T-cell attack unknown synovial joint antigen to cause inflamm

Multiple sclerosis

type 4 T-cell attacks myelin and proteolipid protein causing brain degenerate and paralysis

Rheumatic fever

2-3 weeks following S. pyogenes (strep) Aby cross reacts with heart tissue causing inflamm in heart, joints and kidneys

Lyme disease

From Borrelia bacteria in tick bites, causes bullseye rash and can be treated with doxycycline can show signs of neurological Sx/fatigue and predispose you to autoimmune arthritis

Linkage disequilibrium

HLA proteins in the polymorphic and highly polymorphic group have more of a chance to predispose you to a certain disease

Type 1 intravenous response

vascular permeability increase leading to circulatory collapse Tracheal occlusion

Type 1 SC response

wheal and flare reaction from increased swelling

type 1 inhaled (nose)

congestion, irritation, hay fever

type 1 inhaled (lungs)

bronchial constriction, increased mucus, asthma

type 1 food allergy

vomiting, pruritis, urticaria, anaphylaxis

penicillin Rx

can cause type 2 (cytotoxic) reaction by attaching to RBC instead of tranpeptidase. marking it for Aby and destruction