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

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

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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
T-regulator cells * Activation dependent on? * Activation causes? * All T-reg cells express
* 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 _***
26
**Ankylosing Spondylitis**
HLA **B27= **inflammation leads to fusion of verterbal discs.
27
MS HLA allotype
DQ 6
28
**Ciliac Disease**
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!***
29
Infection and autoimmunity
**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
30
Infections that cause \_1-5\_\_\_, HLA type? 1. Rheumatic fever 2. Reiter's syndrome 3. Reactive arthritis 4. Chronic arthritis 5. Type 1 Diabetes
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
31
Why do infections increase autoimmunity?
IFN-gamma induction= incrased MHC II expression on tissues= t-cell activation and autoummunity
32
Autoimmune hemolytic Anemia - treatment?
**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
Immune thrombocytopenic purpura
Type 2 Autoimmune * Antibodies attach blood platelets * decreases in platelets--\> purpura (bleeding)
34
Goodpastures Syndrome- what is it? treatment?
**_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
Diabetes Type I
Insulin dependent= type II and IV autoimmune * antibodies to beta cell surface, cytoplasmic antigen, * HLA DR3, 4
36
**_Hashimotos_** * What is it * What does it cause? * Treatment?
Type II and IV (TH1 response) * Antibodies to thyroglobulin and thyroid peroxidase * Hypothyroidism * **Treatment:** oral thyroid hormone
37
Addison's Disease
failure to make cortisol and mineralcorticoids
38
**_Grave's Disease_** Cause, Sx, treatment
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
**_Pernicious Anmeia_**
anti-**parietal cell** antibodies, anti-**intrinsic factor** antibodies= Type Impaired B12 bsorption because of lack of intrinsic factor= decreased thymine synthesis
40
**_Autoimmune Chronic active Hepatitis_**
* Liver expresses MHC II proteins= **anti-liver antibodies** * HLAB8, DR3
41
Rheumatoid arthritis- type? factors? * Synovial fluid contains? * Factors? * Treatment? * What makes it worse?
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
Butterfly rash? Epidemiology?
Systemic lupus erythematous= african and asian women IgG antibodies to histone, DNA, (cell compenents)
43
Weakness and tingling in legs--\> paralysis and inability to breath 1. **What is it?** 2. **Treatment?** 3. **What type of immune problem? **
1. **Guillain Barre**= peripheral nerve demyelination. 2. **Treat:** plasmaphoresis, high dose immunoglobulin therapy 3. **Type II and IV autoimmunity**
44
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
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. 1. **Acute disseminated encephalomyelitis** 2. Type IV 3. after infection or vaccine
45
Antibodies to Ach receptors 1. Disease 2. Type of autoimmune 3. sx 4. treatment
1. **Myasthenia Gravis-** antibodies to AchR at neuromuscular junction 2. Type II autoimmune 3. severe muscle weakness 4. Cholinesterase inhibitor, immunosuppressive drugs, thymectomy
46
**Type I Hypersensitivity ** Mechanism, Examples?
**Allergies= IgE crosslinking** * Atopic Triad= asthma, atopic dermatitis, allergic rhinitis (hay fever * food allergies * insect bites/stings
47
Parts of an allergic reaction?
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
Mast cells 1. come from? Cytokines that induce production? 2. Affinity for? 3. Live in? 4. Activation? 5. Molecules released?
**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
* FcER1 Receptor domains * what binds FcER1?
* 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
FcER1 vs FcER2
* **FcERI= high affinity**- Basophils, mast cells * **FcERII= **B-cells, T-cells, monocyts, follicular dendritic cells
51
Histamine 1. **Production** 2. **Receptors--**where are they found? 3. **Anti-histamine drugs? Drowsiness? ** 4. **MOA?**
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
Basophils 1. Receptor 2. Secretion=Role
1. FcERI 2. Secrete IL-4, IL-13= TH2 differentiation
53
LTC4
**Leukotriene C4**= increased vascular permeability, increased mucousal secretion, smooth muscle contraction = anaphylactic shock
54
Atopy
Genetic predisposition for IgE production
55
IgE class switching from? It binds?
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
Inhaled allergens- 1. examples 2. common features
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
**Sensitization to allergen**
= 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
Allergen route of entry alters response--IgE/Mast cells response 1. IV 2. Subcutaneous 3. Inhalaed (x2) 4. Oral
1. IV= systemic anaphylaxis: edema, tracheal occlusion, circulatory collapse, death 2. Wheal and flare- LOCAL increase in permeability and blood flow 3. * Allergic Rhinitis- edema of nasal mucosa * Bronchial astham- bronchial constriction from dust mite feces and pollens 4. Vomiting, diarrhea, itching, hives, anaphylaxis
59
Methods to diagnose allergies (x3)
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
Systemic Anaphylaxis= 3 parts Treatement?
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
Penicillin
**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
Allergic Rhinitis
1. allergin enters mucosa, activates **LOCAL** mast cells 2. increased blood velle permeability, epithelial activation 3. Eosinophils enter nasal passage
63
Allergic Asthma- types, mechanism
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
Clinical presentation of asthma
* Wheezing, coughing, hypersensitve airways, * Thickened smooth muscle, * eosinophils, mast cells, T-cells and mucous all found in airway
65
Treatment for allergic reactions? (3 things)
1. Avoidance 2. Drugs 3. Desensitization
66
Drugs for Allergice reactions
1. Inhibitors of inflammation= corticosteroids, anti-LTC4-R, chromolyn sodium (prevent mast cell degranulation) 2. Bronchodilators 3. Antihistamines 4. Anti-IgE
67
**Desensitization**- mechanims, risk?
* increase allergen doses to shift response to Th1 or induce IL-10/TGFbeta Tregs * Risk: induce allergy or type III hypersensitivity
68
**_Type II hypersensitivity- mechanism_** * **_major ones_**
**immune cells bind proteins on cell surfaces** * Drugs causing hemolytic anemia, thrombocytopenia * ABO antigen reactions, Rhesus factor *
69
Rhesus factor immunization?
* 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
**Type III Hypersensitivity**
**Immune complexes of IgG and SOLUBLE antigens, COMPLEMENT ACTIVATION!** 1. **Early**- Antibodies
  • Intermediate- Ab=Ag, large complex form, complement fixation, cleared from circulation
  • Late- Antibodies>antigens. Medium complexes form, complement fixation, cleared from circulation
    • 71
    **Type III Hypersensitivity- **Disease depends on route * IV * Subcutaneous * Inhaled
    Sx depend on where immune complexes go. * **IV-** vasculitis (Blood vessels), nephritis (renal glomeruli), arthritis (joint spaces) * **Subcutaenous=** arthus * **Inhaled=** farmer's lung
    72
    **_Arthus Reaction_**- What type? * Symptoms * MOA
    **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
    **_Serum Sickness_**- type? * Sx? * Causes?
    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
    Chronic infections can cause?
    Type III- formation of immune complexes. * Injury to blood vessels, nerves, skin and kidneys * Ex: Subacute bacterial endocarditis,
    75
    **_Farmer's Lung-_** * **Type? ** * **Sx? **
    * **Type III-** inhaled antigen caues IgG response= immune complexes form in lungs * **Sx:** difficulty breathing, can cause irreversible damage to alveolar membranes.
    76
    Chronic Autoimmune disease causing Type III (X2)
    **Rheumatoid arthritis-** deposit of immune complexes in joints **Systemic lupus erythematosus**- immune complexes against nuclear antigens

    Immunology (12 decks)

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