Asthma pathogenesis involves airway dendritic cells presenting inhaled antigens to T helper 2 cells, causing them to release cytokines like IL-4, IL-5, and IL-13. These cytokines promote eosinophil development, mucus secretion, airway hyperresponsiveness, and IgE production by B cells. IgE then binds to mast cells and basophils via FcεRI receptors, making them sensitive to allergens and able to release inflammatory mediators. Omalizumab works by binding to free IgE via its Cε3 domain, preventing IgE from binding to mast cells and basophils.

1. Pathogenesis of
asthma

2. Pathogenesis of
Br Asthma
antigens
Air Way
EP
I
DC
DC
DC
G
C
G
C
Interstitium
Cytokines
release
Th2
IL-4
IL-5
IL-13

3. Causes
eosinophilia
IL-4
IL-5
IL-13
IL-13 also causes:
IL-4
IL-13
B Cell
 Inc. mucus
secretion
Mast
Cell
 Hyperresponsiveness
IgE release
Activation
&
Converted
to
Plasma
cells
Basphil

4. Cytokines release
IL-4
Mast
Cell
B Cell
IgE release
Plasma
cells
Basphil

5. Mechanism of
action of Omalizumab
Bound Ig E
Mast
Cell
Free Ig E
FcεRI receptor
Cε3 domain
Basphil
Omalizumab binds
to free IgE with Cε3
domain

6. Mechanism of
action of Omalizumab
Bound Ig E
Mast
Cell
FcεRI receptor
Basphil