Lecture 25 Flashcards
Skin allergies are caused by:
the release of histamine into the tissue from mast cells in the skin.
Oedema is caused by:
Leakage of fluid into the spaces between cells.
ANaphylaxis and anaphylatic shock:
When oedema and swelling occurs at multiple anatomical sites that are distant from the original site of allergen challenge. The treatment is immediate injection of adrenaline (epinephrine)
Type I hypersensitivity
Atopic allergy (IgE mediated) - immediate
Type II hypersensitivity:
Complement mediated - medium
Type III hypersensitivity
Serum sickness (Immune complexes) medium
Type IV hypersensitivity
Delayed Type (DTH) slow response
The receptor for IgE in type 1 allergy:
FcER receptor on mast cells.
How does Type I occur?
The FcER receptor on mast cells has very high affinity towards IgE: antigen complexes. When IgE binds large complex antigens (like pollen), it triggers local mast cells to rupture and empty their granules. Powerful inflammatory mediators are released causing an allergic reaction.
Type II hypersensitivity involves:
FcR, complement, and neutrophils
Rhesus baby - acute haemolytic anaemia
This condition is caused by a blood group antigen RhD on the surface of red blood cells. Maternal antibodies developed to fetal RhD cause lysis of newborn RBCs.
Treatment or allergy for Rhesus anaemia
Make high affinity IgG that competes IgE. Skin scratch test identifies the allergy.
Monoclonal antibodies:
A consequence of research on affinity maturation. Separate individual B cells from an immunized mouse to study somatic hypermutation
Pros of monoclonal antibodies as therapeutic agents:
Highly specific, so no off target effects, humanised, so they stay in the blood stream for months, no adverse reactions to the antibody, can be modded for even greater potency.
Cons of MAB
Expensive to develop and make commercially, side effects of their function can be serious.
