Several mechanisms have been postulated to explain the pathogenesis of the differentiation syndrome. Molecules such as cathepsin G that are known to increase capillary permeability, and cell surface adhesion molecules such as CD15s and the integrins (CD 11a and CD11b) are implicated in the pathogenesis of this syndrome.68 Increased expression of IL-1 on the APL cell induces ICAM-1 and VCAM-1 expression on the vascular endothelium, which in turn enhances leukemic cell binding to the endothelium.69 Cytokines, including TNF-a, IL-6, and IL-1p, may contribute by promoting leukocyte activation.7071

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