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Immunology > Hypersensitivity Type 1-4, autoimmunity (2 lectures) > Flashcards

Hypersensitivity Type 1-4, autoimmunity (2 lectures) Flashcards

1
Q

Type I hypersensitivity- cell type, mediator, antigen, example

A

Antibodies mediated= IgE to allergens. Ex: allergic rhinitis, asthma, peanut allergy

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2
Q

Type II hypersensitivity- cell type, mediator, antigen, example

A

Antibodies, IgG= insoluble antigens Ex: drug allergies (penicillin),

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3
Q

Type III hypersensitivity- cell type, mediator, antigen, example

A

Antibodies, IgG, IgM= soluble antigens

Ex: serum sickness, arthus

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4
Q

Type IV hypersensitivity-

  • cell type/ mediator,
  • antigen,
  • example
A
  • T-cell mediated,
  • soluble and insoluble antigens
  • Ex: TB, contact dermatitis, poison Ivy
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5
Q

Transplant reactions

  1. Chronic Rejection
  2. Acute rejection
  3. hyperacute recetion
A
  1. Type III= chronic
  2. Type IV= acute rejection
  3. Type II= hyperacute
  4. Type I= no transplant reaction
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6
Q

Autoimmune hypersensitivity

  1. Type 1
  2. Type 2
  3. Type 3
  4. Type 4
A
  1. Type 1- none
  2. Type 2- Autoimmune hemolytic anemia
  3. Type 3- Systemic lupus erythematosus
  4. Type 4- Type 1 Diabetes
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7
Q

Syndromes associated with Type 4 hypersensitivity (x3)

A
  1. Delayed type
  2. Contact hypersensitivity
  3. Gluten sensitive enteropathy
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8
Q

Delayed Type Hypersensitivity

A

(ex: poison ivy= pentadecacatechol)

  • Initial exposure=Phase 1: Professional APC take up antigen–> lymph node–> activation of memory T-cells
  • Second+ exposures= Phase 2: APC takes ag to lymph node, memory t-cells migrate to Ag and release cytokines= edema
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9
Q

Memory T-cells induce

A
  • phagocyte recruitment,
  • inflammation,
  • cytokine production.
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10
Q

Langerhans Cells- location, function, lineage

A
  • Fx: In epidermis, immature DC take up antigen= maturation and deliver Ag to lymph node via afferent lymph vessels
  • Lineage: Monocytes, CSF-1 stimulation
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11
Q

Lymphocytes migration?

A

Skin lymphocytes have

  • CLA (cutaneous lymphocyte antigen),
  • P/E selectin ligands, and
  • CCR4, CCR8 and CCR10

to help lymphocytes migrate from lymph node to infection.

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12
Q

Th1 Cell cytokines

A

(memory T-cell following delayed HS reaction) Release:

  • ** IFN gamma- **macrophage activation
  • Chemokines- macrophage recruitment to site
  • TNF-alpha and LT (lymphatoxin)- inflammation, increased expression of adhesion molecules on blood vessels
  • IL-3 and GM-CSF-monocyte production
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13
Q

**Macrophage death at inflammation site? **

A
  • **cytotoxin lymphotoxin- **released by TH1 cells (cytotoxin)- kills macrophages
  • FasL= ligand on T-cell, binds macrophages and kills them
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14
Q

Keratinocyte

  • Activation?
  • Release?
A
  • Activated by: IL-1 (make cytokines), IFN-Gamma (contraction)
  • Release:
    • IL1- fever
    • TNFalpha-cell activation, increased adhesion cell molcule experssion (inflammatory)
    • IL-8- neutrophil chemokine
    • IP-9-?
    • MIG-?
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15
Q

Treatment for contact hypersensitivity?

A

Corticosteroids- suppress inflammation and immune activation

  • Synthesis of anti-inflammatory proteins
  • Suppress cytokines, chemokines, adhesion molecules, inflammatory enzymes, receptors and proteins
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16
Q

Gluten sensitivity Enteropathy

A

Type 4 Hypersensitivity Syndrome

antigen=Gliadin= T-cells attack==> atrophy of villi in small intestine= malabsorption

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17
Q

Difference between delayed type HS and contact HS with regards to Ag

A
  • Delayed- protein injected into skin=TB
  • Contact- small, absorbed into skin = nickel sensitivity, hapten, poison ivy- acts as hapten
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18
Q

Type II Autoimmunity- what is it? Examples?

A

IgG to insoluble antigen

Ex: Graves disease, rhematic fever, Type II diabetes

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19
Q

Type III autoimmunity

A

Immune complex

  • subacute bacterial endocarditis- bacterial antigen causes glomerulonephritis. Strep
  • **mixed essential cryoglobulinemia- **rheumatoid factor IgG complex
  • Systemic lupus erythematosus​-antibodies to DNA, histones, etc
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20
Q

Type IV autoimmunity

A

T-cell mediated (TH1, TH2, CTL)

  • Type 1 diabetes
  • Rheumatoid arthritis
  • MS
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21
Q

Immunological self-tolerance (x6)

A
  1. Negative selection of B-cells in bone marrow
  2. Tissue specific antigen presentation in thymus for negative selection
  3. Immune barriers: brain, eye, testes
  4. anergy of autoreactive b/t-cells in periphery
  5. Regulatory t-cells (CD4+, CD25+) suppress immune response
  6. Limited expression of MHC II and B7 molecules
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22
Q

5 factors thac increase suceptibility to autoimmune diseases

A
  1. HLA genotype
  2. Microbial infection (increased MHC/B7 molecules, molecular mimicry, activation of immune cells)
  3. Injury- cryptic autoantigen presentation immune privledged zones= eyes, testes
  4. Environmental factors= smoking (increased inflammation, ROS, etc), hygeine
  5. Gender and sex homrones: female>male
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23
Q

Sympathetic opthalmia

A

Trauma in one eye can elicit autoimmune response to both eyes (exposure of normally immune restricted auto-antigens)==> blindness in both eyes

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24
Q

Gene mutation that is related to increased autoimmune diseases? (x2)

A
  1. AIRE= AutoImmune REgulator gene= contributes to negative selection in developing T-cells
    • Not all tissue specific antigens are made in thymus
    • Leads to APECED- autoimmune attack of organs and tissues (usually endocrine glands)
  2. IPEX- No FoxP3 expresion on T-reg cells
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25
Q

T-regulator cells

  • Activation dependent on?
  • Activation causes?
  • All T-reg cells express
A
  • T-regulatory cells (CD4+, CD25+) require certain bonds:
    • CTLA-4 on T-reg binds B7 on APC
    • TCR binds MHCII and antigen
  • t-cells (t-reg) recognize self antigen on MHC II and **supress naive t-cell proliferation (CD4+, CD28 binds B7, TCR) **and autoinflammatory cytokines IL-4, IL-10, TGF-Beta.
  • _FoxP3 _
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26
Q

Ankylosing Spondylitis

A

HLA **B27= **inflammation leads to fusion of verterbal discs.

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27
Q

MS HLA allotype

A

DQ 6

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28
Q

Ciliac Disease

A

Autoimmune destruction of intestinal villi= Type IV

  • CD4+ t-cells respond to peptide from gluten degradation (deamination)
  • Presnted by HLA-DQ8/2 molecules
  • Activation of macrophages and B-cells
  • IgG/A antibodeies to translutaminase, gliadin

DQ is the only thing better than pasta!

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29
Q

Infection and autoimmunity

A

Molecular mimicry= Strep antibodies react with heart tissue= **rheumatic fever. **

  • Naive T-cell activated by strep pathogen peptide
  • TH1 responds to pathogen–> macrophage activation= inflammation
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30
Q

Infections that cause _1-5___, HLA type?

  1. Rheumatic fever
  2. Reiter’s syndrome
  3. Reactive arthritis
  4. Chronic arthritis
  5. Type 1 Diabetes
A
  1. Group A strep, unknown
  2. Chlamydia= HLA-B27
  3. Camp jejuni, shigella, salmonella, yersinia, HLA-B27
  4. Lyme disease- DR2,DR4
  5. CoxA, CoxB, echo, rubella= DR3
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31
Q

Why do infections increase autoimmunity?

A

IFN-gamma induction= incrased MHC II expression on tissues= t-cell activation and autoummunity

32
Q

Autoimmune hemolytic Anemia

  • treatment?
A

**Type 2 autoimmune **

Erythrocytes are bound by antibodies=

  • destruction in spleen (phagocytosis and lysis)
  • scomplement activation in spleen (phagocytosis and lysis)
  • complement activation and intravascular hemolysis

Treatment: splenectomy

33
Q

Immune thrombocytopenic purpura

A

Type 2 Autoimmune

  • Antibodies attach blood platelets
  • decreases in platelets–> purpura (bleeding)
34
Q

Goodpastures Syndrome- what is it? treatment?

A

Type 2 Autoimmune

  • IgG against Type IV collagen (alpha 3 chain) in basememnt membrane of LUNGS and KIDNEYS
  • renal glomeruli most effected
  • **Treatment: **plasma exchange and immunosuppressive drugs
35
Q

Diabetes Type I

A

Insulin dependent= type II and IV autoimmune

  • antibodies to beta cell surface, cytoplasmic antigen,
  • HLA DR3, 4
36
Q

Hashimotos

  • What is it
  • What does it cause?
  • Treatment?
A

Type II and IV (TH1 response)

  • Antibodies to thyroglobulin and thyroid peroxidase
  • Hypothyroidism
  • Treatment: oral thyroid hormone
37
Q

Addison’s Disease

A

failure to make cortisol and mineralcorticoids

38
Q

Grave’s Disease

Cause, Sx, treatment

A

Agonistic antibody to TSH receptor

  • Sx: exophthalmos, irritibility, warm skin, weight loss
  • Treat: thyroidectomy, destruction with radioactive I
  • CAN BE PASSED TO INFANT (IgG)!!!
39
Q

Pernicious Anmeia

A

anti-parietal cell antibodies, anti-intrinsic factor antibodies= Type

Impaired B12 bsorption because of lack of intrinsic factor= decreased thymine synthesis

40
Q

Autoimmune Chronic active Hepatitis

A
  • Liver expresses MHC II proteins= anti-liver antibodies
  • HLAB8, DR3
41
Q

Rheumatoid arthritis- type? factors?

  • Synovial fluid contains?
  • Factors?
  • Treatment?
  • What makes it worse?
A

Type III and Type IV= IgM/IgG or IgA against Fc region of IgG

  • Synovial fluid: CD4T, CD8, B-cells, neutrophils, macrophages
  • **Factors: **PMNs, TH1, TC, IL-1, TNFalpha, IL8, PGE2, LTB4
  • Treatment: anti-inflammatory and immunosuppressive drugs (anti-TNFalpha); AntiCD20 (b-cells have this)
  • Smoking= ciruilline residues- activation of CD4 T-cells–> RA
42
Q

Butterfly rash?

Epidemiology?

A

Systemic lupus erythematous= african and asian women

IgG antibodies to histone, DNA, (cell compenents)

43
Q

Weakness and tingling in legs–> paralysis and inability to breath

  1. What is it?
  2. Treatment?
  3. **What type of immune problem? **
A
  1. Guillain Barre= peripheral nerve demyelination.
  2. Treat: plasmaphoresis, high dose immunoglobulin therapy
  3. Type II and IV autoimmunity
44
Q

Antibodies to MBP and PLP of myelin

  1. Disease
  2. Type of immune problem
  3. Characteristics/Sx
  4. Treatment

Antibodies just to MBP of myelin?

  1. Disease
  2. Type of immune problem
  3. Characteristics
A
  1. Multiple Sclerosis- TH17 or TH1 cells- inflammation leads to demyelinations
  2. Type II and IV
  3. “plaque formation”, motor weakness, impaired vision, lack of coordination, spasticity
  4. Treatment: BLock IL2Ra, and t-cell activation, t-cell migration or proliferation.
  5. Acute disseminated encephalomyelitis
  6. Type IV
  7. after infection or vaccine
45
Q

Antibodies to Ach receptors

  1. Disease
  2. Type of autoimmune
  3. sx
  4. treatment
A
  1. Myasthenia Gravis- antibodies to AchR at neuromuscular junction
  2. Type II autoimmune
  3. severe muscle weakness
  4. Cholinesterase inhibitor, immunosuppressive drugs, thymectomy
46
Q

**Type I Hypersensitivity **

Mechanism, Examples?

A

Allergies= IgE crosslinking

  • Atopic Triad= asthma, atopic dermatitis, allergic rhinitis (hay fever
  • food allergies
  • insect bites/stings
47
Q

Parts of an allergic reaction?

A
  1. Sensitization=
    • Production of: Th2 CD4 T-cells, IgE
    • IgE binding FceRI on mast cells and basophils
  2. Effector Phase
    • Acute= mast/basophil degranulation
    • Chronic=influx of TH2 cells and eosinophils and degranulation of eosinophils
48
Q

Mast cells

  1. come from? Cytokines that induce production?
  2. Affinity for?
  3. Live in?
  4. Activation?
  5. Molecules released?
A

Mast cells

  1. Hemopoietic stem cells-CD117, SCF (stem cell factor)
  2. high affinity for FcER1
  3. Live in mucosal and epithelial tissue linings
  4. IgE crosslinking causes conformational change= degranulation
  5. 2 phases
    • preformed: TNF-alpha, histamine/heparain, enzymes
    • Synthesis of: IL4, IL13; IL3, 5; CCL3; Leukotriene C/D/E; platelet activating factor.
49
Q
  • FcER1 Receptor domains
  • what binds FcER1?
A
  • Domains:
    • Alpha1 and Alpha 2 chains= Antibody binding domain
    • ITAM= immunotyrosine activation domain- has beta and two gamma transmembrane chains. _Gamma chain= intracellular signaling _
    • IgE C2/C3 domains bind at alpha1/2 domains of FcER1
  • **Mast cells and basophils bind **
50
Q

FcER1 vs FcER2

A
  • FcERI= high affinity- Basophils, mast cells
  • **FcERII= **B-cells, T-cells, monocyts, follicular dendritic cells
51
Q

Histamine

  1. Production
  2. Receptors–where are they found?
  3. **Anti-histamine drugs? Drowsiness? **
  4. MOA?
A
  1. Histidine +decarboxylation= histmaine
  2. H1-H4. H1 in endothelial cells, smooth muscle cells (myosin light chain kinase), nerve cells, hematopoietic cells
  3. Block decarboxylation—if they don’t cross BBB then they won’t cause drowsiness
  4. **Receptors cross link= kinase cascade, calcium mobilization==> arachidonic acid pathway and myosin phosphorylation **
52
Q

Basophils

  1. Receptor
  2. Secretion=Role
A
  1. FcERI
  2. Secrete IL-4, IL-13= TH2 differentiation
53
Q

LTC4

A

Leukotriene C4= increased vascular permeability, increased mucousal secretion, smooth muscle contraction

= anaphylactic shock

54
Q

Atopy

A

Genetic predisposition for IgE production

55
Q

IgE class switching from? It binds?

A

IL-4= secreted from basophils, mast cells

  • **activation of mast cells= IL-3/5==> **eosinophil production= toxic, makes more IL-3/5, cytokines cause mast cell degranulation
  • =Activation of basophils= IL-4/IL-13==> TH2 + IgE class switching
    • TH2= IL-5==>eosinophil production and activation
    • IgE binds mast cells and basophils
56
Q

Inhaled allergens-

  1. examples
  2. common features
A
  1. pollen, dust mite feces, cockroach feces
  2. proteins (proteases) that
    • induce Th2 response with
    • low MW, high solubility to allow diffusion into mucous.
    • VERY STABLE
    • peptides bind MHC II
57
Q

Sensitization to allergen

A

= first exposure

  • Allergen penetrates barrier
  • APC presents to naive t-cell==> TH2 class
  • TH2 secreted IL-4
  • B-cells class switch==> IgE antibody production
58
Q

Allergen route of entry alters response–IgE/Mast cells response

  1. IV
  2. Subcutaneous
  3. Inhalaed (x2)
  4. Oral
A
  1. IV= systemic anaphylaxis: edema, tracheal occlusion, circulatory collapse, death
  2. Wheal and flare- LOCAL increase in permeability and blood flow
    • Allergic Rhinitis- edema of nasal mucosa
    • Bronchial astham- bronchial constriction from dust mite feces and pollens
  4. Vomiting, diarrhea, itching, hives, anaphylaxis
59
Q

Methods to diagnose allergies (x3)

A
  1. skin testing- 3 parts= allergin, saline (volume control), histamine (positive control)
  2. total serum IgE (should be low if healthy)
  3. Antigen specific IgE with RAST or ELISA assay
60
Q

Systemic Anaphylaxis=

3 parts

Treatement?

A

Antigen enters blood stream and activates mast cell degranulation

3 parts

  1. CV System- edema, low bp, low o2, irregular heartbeat, loss of conciousness
  2. Respiratory tract-smooth muscle contraction ==>difficulting swallowing, breathing, wheezing
  3. GI tract- smooth muscle contraction= stomach cramps, vomiting, fluid outflow into gut, diarrhea

**Treatment- epinephrine works to raise BP from 40-80 within 10 minutes **

61
Q

Penicillin

A

**Type I Reaction: **Hapten- beta ring open and binds proteins

Type II reaction: penicillin modifies proteins on surface of erythrocytes, complement coating. APC present modified self-erythrocyte antigen= TH2 response.

62
Q

Allergic Rhinitis

A
  1. allergin enters mucosa, activates LOCAL mast cells
  2. increased blood velle permeability, epithelial activation
  3. Eosinophils enter nasal passage
63
Q

Allergic Asthma- types, mechanism

A

Extrinsic= IgE mediated, Intrinsic= idiopathic

Acute

  • (sensitized people) IgE coated mast cells for specific antigen==>cross-linking/activation of mast cell
  • release of cytokines= increased vascular permeability, mucous secretion, smooth muscle contraction

Chronic

  • influx of inflammatory cells (eosinphils, Th2)= more cytokine production and loop.
64
Q

Clinical presentation of asthma

A
  • Wheezing, coughing, hypersensitve airways,
  • Thickened smooth muscle,
  • eosinophils, mast cells, T-cells and mucous all found in airway
65
Q

Treatment for allergic reactions? (3 things)

A
  1. Avoidance
  2. Drugs
  3. Desensitization
66
Q

Drugs for Allergice reactions

A
  1. Inhibitors of inflammation= corticosteroids, anti-LTC4-R, chromolyn sodium (prevent mast cell degranulation)
  2. Bronchodilators
  3. Antihistamines
  4. Anti-IgE
67
Q

Desensitization- mechanims, risk?

A
  • increase allergen doses to shift response to Th1 or induce IL-10/TGFbeta Tregs
  • Risk: induce allergy or type III hypersensitivity
68
Q

Type II hypersensitivity- mechanism

  • major ones
A

immune cells bind proteins on cell surfaces

  • Drugs causing hemolytic anemia, thrombocytopenia
  • ABO antigen reactions, Rhesus factor
    *
69
Q

Rhesus factor immunization?

A
  • During first pregnancy of Rh- mother with Rh+ fetus, Anti-Rh IgG is given to mother.
  • Fetal erythrocytes are bound by Anti-Rh IgG which prevents activation of B-cells= no antibodies formed.
  • Future Rh+ pregnancies are safe.
70
Q

Type III Hypersensitivity

A

Immune complexes of IgG and SOLUBLE antigens, COMPLEMENT ACTIVATION!

  1. Early- Antibodies <ag>
    </ag><li>
    <strong>Intermediate-</strong> Ab=Ag, large complex form, <strong>complement fixation</strong>, cleared from circulation</li><li>
    <strong>Late-</strong> Antibodies&gt;antigens. Medium complexes form, <strong>complement fixation, cleared from circulation </strong>
    </li>

</li>
</ag>

71
Q

**Type III Hypersensitivity- **Disease depends on route

  • IV
  • Subcutaneous
  • Inhaled
A

Sx depend on where immune complexes go.

  • IV- vasculitis (Blood vessels), nephritis (renal glomeruli), arthritis (joint spaces)
  • Subcutaenous= arthus
  • Inhaled= farmer’s lung
72
Q

Arthus Reaction- What type?

  • Symptoms
  • MOA
A

**Type III HS- localized response **

  • Sx: Localized erythema and hard swelling that subsides within a day
  • MOA: injection of soluble antigen draws IgG to specific tissue.= aggregation of mast cells, and antibodies. Complement fixation propogates response. Blood vessel occlusion from platelet accumulation.
73
Q

Serum Sickness- type?

  • Sx?
  • Causes?
A

Type III- formation of immune complexes with IgG

  • **Sx: **chills, fevers, rash, arthritis, vasculitis, sometimes glomerulonephritis
  • **Causes: **chronic treatment with monoclonal antibodies, immunized orse serum

Self-limiting if not repeated infections.

74
Q

Chronic infections can cause?

A

Type III- formation of immune complexes.

  • Injury to blood vessels, nerves, skin and kidneys
  • Ex: Subacute bacterial endocarditis,
75
Q

Farmer’s Lung-

  • **Type? **
  • **Sx? **
A
  • Type III- inhaled antigen caues IgG response= immune complexes form in lungs
  • Sx: difficulty breathing, can cause irreversible damage to alveolar membranes.
76
Q

Chronic Autoimmune disease causing Type III (X2)

A

Rheumatoid arthritis- deposit of immune complexes in joints

Systemic lupus erythematosus- immune complexes against nuclear antigens

Immunology (12 decks)

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