Latephase response

The above mechanism accounts for the immediate allergic reaction; however, in many cases inflammation with ingress of many cell types, including eosinophils, further mast cells, basophils, neutrophils and lymphocytes, occurs within hours of allergen contact. The mechanisms for this depend partly on chemotactic factors released by mast cells, but probably more on cytokine production by T lymphocytes (IL-3, IL-5, IL-10, granulocyte-macrophage colony-stimulating factor (GM-CSF)), macrophages (GM-CSF) and endothelial cells (GM-CSF), together with mast cells (IL-2, IL-3, IL-4, IL-5) (Figure 2). This cytokine network provides the basis for clonal amplification of T cells, B cells and inflammatory cells such as mast cells, basophils and eosinophils. Cells passing in nearby blood vessels are recruited to the site of inflammation, becoming attached to the vascular endothelium, via expressed integrin molecules on the cell surface which interact with receptors such as ICAM-1 and iC3b on the vascular endothelium. Expression of integrins and their receptors is upregu-lated by inflammatory cytokines. The cells then diapedese through the vascular endothelium and migrate down a chemotactic gradient to the site of allergic inflammation.

Histamine. LTs, PGs, PAF

Histamine. LTs, PGs, PAF

Immedinle effects

M8F> PAF. LTs oxygon melabolites

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