Hypersensitivity Reactions (VISUALIZED) - Immunology

Content:
0:00 Introduction
1:48 Type 1 - Immediate Hypersensitivity Responses
11:10 Type 2 - Antibody Mediated Hypersensitivity Responses
16:31 Type 3 - Immune Complex Diseases
18:59 Type 4 - Cell Mediated Reactions

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All information in my immunology videos are from:
- Book: Immunology, Eighth Edition by David Male, Jonathan Brostoff, David Roth and Ivan Roitt
- Additional research in PubMed
- University lecture materials

Hypersensitivity: Excessive immune response

Coombs and Gell classification of Hypersensitivity
- Type 1: Immediate Hypersensitivity Responses
- Type 2: Antibody Mediated Hypersensitivity Responses
- Type 3: Immune Complex Disease
- Type 4: Cell Mediated Reactions

Type 1 Hypersensitivity: IgE mediated Hypersensitivity
- Reactions caused by IgE antibodies on mast cells leading to anaphylatic shock.
- Factors that induce allergy:
- Pollen, Inhale, Particles from animals, milk, fish, direct contact, etc.
- This happens because the eprson has a genetic predisposition to develop an allergic hypersensitivity against the factors
- Procedure of developing Type 1 Hypersensitivity:
1. Inhale pollen
2. Langerhans cells (or other phagocytes) phagocyte the pollen and then travel through afferent lymph vessel to the lymph node
3. In lymph node:
1. Professional APC will present the pollen on an MHCII to a naive T helper cell. The 3 activation signals help it differentiate (TCR-MHCII, CD28-B7 and IL4), IL2 will help it grow then the Th0 will differentiate into effector Th2 which express CD40L and release Interleukins.
2. B-cell that reacts with a pollen will undergo Receptor mediated endocytosis and meet an effector T helper cell (or a naive Th0) to differentiate. This stage is called Sensitization Stage
4. Sensitization stage lasts for about 6 months to 5 years.
5. Second time we inhale pollen (2nd exposure), pollen will bind to IgE antibodies on mast cells.
6. Mast cells release Histamin which cause vasodilatation, increase permeability of capillaries and also cause bronchoconstriction
7. It will also secrete chemotactic factors like IL5 and TNF-a

Type 2:
Antibody mediated immune response against cell surface antigens
Possible reasons for Type 2 Hypersensitivity:
- Complex Viruses (Viral Budding): During their reproductive cycle, they produce parts of the virus which gos to the surface of the cell to prepare for the viral budding. Antibodies can bind to the antigens on the surface of the cell in meantime.
- Transfusion Reaction: Blood types can react with eachothers Red Blood Cells if the ABO antigens are not correctly transfered
- Drug Allergies
- Autoimmune Reactions (T-Cell tolerance): If T-Lymphocyte escape the central tolerance in the thymus, and they also escape the peripheral tolerance in the extrathymus - autoimmune disease

What happens if Antibody binds to a cell:
- Activation of Classical pathway of Complement System: We'll get both membrane attack complex (MAC) and also C3b will opsonize the cell so Phagocytes can bind to the cell through C3b receptor
- Neutrophils and Natural killer cells can also bind.

Type 3 Hypersensitivity:
Immune Complexes formed in the blood stream
IgM or IgG can bind to a free floating antigen, which can be systemic in the blood or local in a certain area
- Normally Immune Complexes in the blood are destroyed by spleen and liver, but sometimes the complement system can get stuck between the endotheliocytes
- Now the antibodies can bind to neutrophils or basophils. Platelets can aggregate, Mast cells can react. All of this is called Arthurs Reaction
- Serum Sickness disease is also a type of type 3 hypersensitivity. This is when a snake for example bites and secretes their antigens into the bloodstream. If we're quick enough we can inject anti-snake antibodies and we'll get free floating antibodies

Type 4 hypersensitivity:
Th1 and Tcyt cause local inflammation of the skin.
- Tuberculin Skin test (Mantoux test) -
1. inject Tuberculin in the skin and it'll get phagocytosed by a phagocyte
2. Langerhans cell will go to lymph node
3. It'll activate a naive T-helper cell through 3 activation signals.
4. At the same time it'll present the tuberculin on an MHC class 1 which will bind to a naive T cytotoxic lymphocyte. The Tcyt will get activated by receiving IL2 and iFN gamma which will make it into Effector T-cyt cell which will express Fas-Ligand which will bind to Fas and release Perforins and Granzymes.
5. After sensitization stage, the 2nd exposure will happen where Effector Tcyt cell and Th1 are. The Phagocyte will activate them. Th1 will release IFNg which will activate Macrophage. T-cytotoxic cell will also kill cells which have tuberculin between cells.

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