Whats the difference between immunity and hypersensitivity
Immunity is fighting the infection which is a good thing whereas hypersensitivity is when the immune response causes damage to the host tissue which is harmful to the health of the individual
Table he mentioned. This is a big chunk of this module
Fishback's description of Anaphylaxis
1. IgEs are pre made, that is they are made before the superantigen exposure take place.
2. Cell injury is attributed to Th2 cells
3. Ployclonal response
4. Degranulation: antigen binds with IgE then crosslinks with another IgE causing degranulation of mast cells which release mainly histamine.
What is released in Anaphylaxis
1. Mast cells releases histamine, protease and chemotactic factors
2. Cytokines are made IL-1,3,4,5,6
3. Products of arachidonic acid: Prostaglandins and leukotrienes.
4. PAF (he said it is more powerful than histamine)
What happens in the first exposure in regards to Anaphylaxis
Mast cells are loaded up with IgEs
What counteracts the histamine released by mast cells
Eosinophils make histaminase to regulate the effects of histamine.
Clinical significance of eosinophils
If there is a patient will elevated blood count of eosinophils then we have to consider 2 conditions
2. Parasitic infections
What are the 2 components that characterize the anaphylaxis
There are 2 parts of the anaphylaxis response:
1. Immediate reaction
2. Late-phase reaction
Immediate reaction is due to the factors discussed previosuly whereas the late phase reaction is mainly due to prostaglandins and leukotrienes
Describe the process of Anaphylaxis in detail
Important thing to note: during the first exposure there is class switching from IgM to IgE
Important: people with chronic asthma since childhood have obstruction and hyperinflation
High power - lungs - asthma
What are the receptors on mast cells to which antigen-bound IgE bind to and cause degranulation
What is a long term pathology associated with type I hypersensitivity reactions
In people with chronic asthma since childhood their lungs undergo remodeling due to chronic inflammation such that the smooth muscles around their bronchioles undergo hypertrophy.
What antibodies are in type II hypersensitivity
IgM or IgG (no IgE!, thats only in type I)
What did Fishback mention about type II hypersensitivity
1. It can cause increase in IgM and/or IgG. This leads to binding and activation and MAC can then be attached to a cell which leads to its lysis.
2. NK cells can be activated by a phenomenon known as the antibody-dependent cell-mediated cytotoxicity
This is a picture of the glomeruli in Goodpasture Syndrome.
1. IgG or IgM antibodies are made against collagen, specifically type IV collagen
2. Collagen IV is found in the basement membrane which is found all over the body but the organs it affects the most are the lungs and the glomeruli
What happens in type III
Antibodies are IgG and IgM but the antigen this time is solouble. Immune complexes are formed, these are most often formed in situ and are filtered out in the capillaries. Skin and kidneys are most commonly affected
What is lupus classified under
Sytemic Lupus Eryhtmatosus is classified under type III
Post Streptococcal Nephrotitus
Remember that in type III it is the neutrophils that are causing the problems since they are recruited as C3a and C5a binds and recruites neutrophils
Explain type IV hypersensitivity reaction
1. Antibodies are not involved at all, T cells are involved specifically Th1 cells.
2. Th1 release cytokines recrutiting more macrophages that form Langhans Giant cells
Explain the structure of a granuloma
1. Langhaans cells shown in U
2. The macrophages inside has more cytoplasm so they appear different
3. Outside are the lymphocytes
4. The whole thing is encapusilated by a fibrous, sometimes calcified fibrous layer.
This is observed in infections like TB and Herpes
Type IV hypersensitivity in the skin
Contact Dermatitus which is a type IV reaction. This picture specifically is for Poison Ivy