inflammation and hypersensitivity. i.now that we know basics about varying forms of cellular and...
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Inflammation and HypersensitivityInflammation and Hypersensitivity
I. Now that we know basics about varying forms of cellular and humoral
cascades, ready to talk more about dysfunction
A. Inflammation can be cellular mediated and/or
humoral and can involve complement and
clotting cascade
B. Text goes over varying complement pathways,
can be classical or alternative.
Players in responses
• The palyers are the same essentially as in blood section and immuno section
These are usually first to inflammation Both in serum and mucosal, will function much as macrophages
Macrophages are later arriving
Monocytes are close relatives and are more plasma oriented
But much of symptomology comes from these
As they release 5HT and histamines and ECP-A
These are usually last even after macros. So if see probably chronic condition
Inflammation has a few aspects
• Is based usually on a response to parasites (may be how it evolved)• Uses IgEs a lot and mast cells and eosinophiles• May also use complement• If long term can encapuslate using clotting cascade
Now Hypersensitivity
• Four types:• I- IgE mediated by allergen• II-tissue specific• III-immune complex• IV-cell-mediated
Type I
• Big Player is histamine which has opposing effects based on which subtype of receptor is activated.
• H1 tend to increase inflammation• H2 tend to ameliorate• H3 are more CNS derived
Histamine Receptors
G-pr- IP3
cAMP
Immune recruitment
Bronchial constriction
Immune silencing via Ts
Gastric secretion
H1
H2
Allergy response
Allergensensitization
IgEMasteosins
H1
II
HLA mismatch CD8
MHCII
Attack complex
Mechanisms of anti self
• Phagocytosis after opsinization
• Complementation
• Tc destruction
• Ab blockade of receptor subtypes
III
allergen
Attack complex
complexation
IV
CD4 or CD8
If CD4 termed delayed
antigen
Antigen presenting cell destroyed either directly or after antigen presentation by host