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