Lesson 9 immuno (page 1) by Sharifah Fahimah https://padlet.com/fahimah_alkaff_fah/mw2dup7ep7838nz Made with a dash of wit en-us 2020-07-14 01:15:36 UTC 2020-07-14 11:38:54 UTC hello@padlet.com Sharifah fahimah_alkaff_fah https://padlet.com/fahimah_alkaff_fah/mw2dup7ep7838nz/wish/653787451 There are 4 types of hypersensitivity: 

Type I: Allergy
1) first exposure (sensitization) 
- Antigens get picked by immune cells (mast cells / dendritic cells) 
- migrate to lymph node to present antigen to T helper cells
- T helper cell 
--> activate B cell --> class switching
--> Th2 cytokines = increase IgE production 

2) Second exposure
- antigen binds to IgE present on the surface of the mast cells 
- mast cells will be activated and degranulate --> release of histamine --> allergic reaction 

Type II: Antibody- dependent killing
- Tissue specific 
- B cell activation and antibody production 
= complement system activation 
= ADCC
= antibody-mediated cellular dysfunction

Type III: Immune complex mediated
- Formed when antibodies bind to SOLUBLE antigens
- Antigen-antibody complex deposits in blood vessels walls 
= Inflammation and tissue damage. 

Type IV: T cell mediated 
- antigen presented on APC 
- TH1 effector T cells cells will recognize antigens in the APC and will release cytokines. 
- Cytokines enhance the killing capability of the macrophages
- recruitment of phagocytes and plasma cells to the site of infection --> visible lesion. 
= Inflammation and tissue damage

]]> 2020-07-14 02:17:57 UTC https://padlet.com/fahimah_alkaff_fah/mw2dup7ep7838nz/wish/653787451 Jun Yi fahimah_alkaff_fah https://padlet.com/fahimah_alkaff_fah/mw2dup7ep7838nz/wish/653788912 The difference between the Type II Hypersensitivity and the Type III hypersensitivity:

- Complement used in small amounts in the type II hypersensitivity while the  complement used in large amount (C3 + C4) in the Type III hypersensitivity 


Type I Hypersensitivity can have mild and severe symptoms:

- Mild symptoms - Hives (urticaria), Eczema, allergic rhinitis, asthma
- Severe symptoms - increase the vascular permeability, airway constriction, can't supply vital organs --> ANAPHYLACTIC SHOCK!

]]> 2020-07-14 02:20:00 UTC https://padlet.com/fahimah_alkaff_fah/mw2dup7ep7838nz/wish/653788912 Wan Teng fahimah_alkaff_fah https://padlet.com/fahimah_alkaff_fah/mw2dup7ep7838nz/wish/653789042 4 types of hypersensitivity:
1. Type I (allergic reaction)
- IgE-mediated
-Antigen is from the environment
-Allergen binds to BCR to induce IgE formation--> Fc receptor of IgE bind to Fce receptor on mast cell surface --> antigen bind to 2 or more IgE on mast cell surface, cross-linking them which signals mast cells to undergo degranulation to release histamine and other inflammatory mediators
-Time of onset: 15-30 mins, sometimes 10-12 hrs

2. Type II (antibody-dependent cytotoxicity)
- Antibody-mediated (usually IgM or IgG)
-Antigen is on cell surface
-IgG bind to cellular antigen, leading to cell lysis by activation of complement system or ADCC (by NK cells)
-Time of onset: minutes to hours

3. Type III
-Immune complex-mediated
-IgG binds to soluble antigens to form antigen-antibody complex, which are deposited in blood vessel walls or various tissues, resulting in pain, inflammation and tissue damage.
-Time of onset: 3-10 hrs after exposure to antigen

4. Type IV (delayed type)
-Cell-mediated (involves B and T cells)
-Time of onset: 48-72 hrs, 3-4 weeks

Type I, II and III involves antibodies, while type IV does not involve antibodies.]]> 2020-07-14 02:20:11 UTC https://padlet.com/fahimah_alkaff_fah/mw2dup7ep7838nz/wish/653789042 Nicole fahimah_alkaff_fah https://padlet.com/fahimah_alkaff_fah/mw2dup7ep7838nz/wish/653789206 Hypersensitivity 
There are 4 types of hypersensitivity. 

Type I (Allergy)
  • Allergen sensitization
  • In the first exposure to an allergen, B cells will be activated to produce IgE to the allergen. 
  • IgE will bind to mast cell surface receptors.
  • When mast cells are activated by the binding, they will release histamine   

Type II (Antibody-dependent killing) 
  • IgG-mediated. 
  • Triggered by cell-associated antigens.
  • B cells activated will produce antibodies. 
  • Antibodies will go through complement activation and causes cellular lysis. 
  • Damage to host tissue caused by cell lysis induced by the direct binding antibody to the cell surface antigens.

Type III (Immune complex-mediated)
  • Injury is mainly due to leukocyte recruitment and inflammation. 

Type IV (Delay Type Hypersensitivity)
  • The antigen is injected into the subcutaneous tissue
  • Pick up by APC
  • TH1 effector cell recognizes antigen and will release cytokines.
  • Phagocyte and plasma will go to the site of antigen injection and causes visible lesion.

]]> 2020-07-14 02:20:24 UTC https://padlet.com/fahimah_alkaff_fah/mw2dup7ep7838nz/wish/653789206 Faith fahimah_alkaff_fah https://padlet.com/fahimah_alkaff_fah/mw2dup7ep7838nz/wish/653789298 4 types of hypersensitivity
Type I: IgE mediated hypersensitivity
- Reaction to most allergies 
- First exposure (sensitization) then subsequent exposure (more serious) 
- Patients usually have genetic predisposition to having over-reactions to allergens / unknown molecules. 
- APC present the allergen to T-helper cells with co-stimulatory molecules 
- T cell differentiates into Type II T helper cells and release interleukin 4, 5, 10. 
- Interleukin 4 causes B cells to undergo class switching and produce IgE instead of IgM.
- Interleukin 5 activates eosinophils which degranulates and kills the cells. 
- IgE binds to mast cells by Fce receptors and is ready for the second exposure. 
Second exposure 
- Mast cells with specific IgE binds to allergen and degranulates, releasing mediators (histamine)
- Histamine binds to H1 receptors and causes the muscles to contract, blood vessel dilation and increase permeability. While blood flow to infected site increases, fluid will leak out easily which causes swelling.

Type II: Cytotoxic hypersensitivity 
- Antibodies bind to antigens on cells surfaces 
* Complement proteins used in small amounts
Mechanism 1: Complement system is activated and activates neutrophils to release oxygen radicals which kills the host cells. 
Mechanism 2: Complement system is activated and MAC is formed in the host cells which leads to apoptosis. 

Type III: Mediated by immune complexes 
- B cells secrete IgG instead of IgM. 
- Antibodies bind to soluble antigens 
- Antibodies bind to self soluble antigens 
- Small antigen-antibody complex are less immunogenic (less attracted to macrophage)
- Small complexes stay in blood longer and activate the complement system 
* Complement protein used in large amounts (C3, C4) 
- Chemokines are release which attracts neutrophils to degranulate and cause inflammation. 
* leads to pain and tissue damage

Type IV: T cell mediated hypersensitivity
-  Antigen is deposited into subcutaneous tissue and is ‘picked up’ by APC and presented to T cells on MHC II molecule
- T cells bind to MHC II molecule by T cell receptor and CD4 co-receptor and express CD28 protein. 
- CD28 protein binds to B7 protein on the surface of APC. 
- APC will release interleukin 12 (cytokine) which causes the naïve T cell to mature and differentiate into Type I helper T cell.
- Type I helper T cell will release IL-2 (cytokine) which will cause itself and other T cells to proliferate.
- More TH1 cells will also be produced by interferon gamma as well as activation of phagocytes like macrophages.
- Macrophages will release pro-inflammatory cytokines like IL-1, IL-6 which will cause leakiness in endothelial barriers and allow more immune cells into the infected site which causes swelling as well as fever. 
- Lysosomal enzymes, complement components and ROS will also be secreted by marcrophages and damages tissue. 

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