Relative Contributions of α₄ and α_L Integrins to IL‐4‐Induced Leukocyte Rolling and Adhesion

Abstract

Following tissue activation with IL-4, alpha4 and alphaL initiate the attachment and deceleration, respectively, of leukocytes during rolling, and are responsible for mediating the adhesion CD4+, CD8+, Gr-1+ leukocytes.

Effects of Histamine on Immunophenotype and Notch Signaling in Human HL-60 Leukemia Cells

“…pI and prevents the attachment of HL-60 cells; from the.endothelium in vitro (23); Some studies 'demonstrated a correlation between high expression' of CD49d and metastasis (24; 25). The upregulation of VLA-4 expression increases the cell interaction with the blood vessels (26). Thus, the reduced expression of CD49d suggests the beneficial effect of histamine in immunotherapy.…”

Differential regulation of surface receptor expression, proliferation, and apoptosis in HaCaT cells stimulated with interferon-γ, interleukin-4, tumor necrosis factor-α, or muramyl dipeptide

“… 39 Alternatively, the IL-4-mediated inhibition of CD49d expression in HaCaT keratinocytes could be a mechanism to downregulate leukocyte adhesion to keratinocytes to control the inflammatory process, since CD49d is known to play a critical role in leukocyte adhesion to other cell types. 40 This phenomenon may also reflect a mechanism by which the keratinocyte response to locally released IL-4 attempts to control excessive inflammatory processes such as AD.…”

The p110δ Isoform of PI3K Differentially Regulates β1 and β2 Integrin‐Mediated Monocyte Adhesion and Spreading and Modulates Diapedesis

“…The necessity of both integrins, LFA‐1 and VLA‐4, for leukocyte adhesion and spreading in vivo has been demonstrated in an interleukin‐4‐induced inflammation model ( 50 ). Firm adhesion and spreading of monocytes on the surface of the endothelium requires functional LFA‐1 and VLA‐4 binding to their receptors ICAM‐1 and VCAM‐1 expressed on activated endothelium ( 50 ). In fact, during diapedesis leukocytes form integrin‐mediated adhesions at their leading edge while co‐ordinately disassembling integrin assemblies at their rear, which has been shown to be regulated by chemokines ( 51,52,53 ).…”

“…During the formation of atherosclerotic plaques, macrophages accumulate in the tunica intima of vessels as a consequence of diapedesis of peripheral blood monocytes ( 49 ). The necessity of both integrins, LFA‐1 and VLA‐4, for leukocyte adhesion and spreading in vivo has been demonstrated in an interleukin‐4‐induced inflammation model ( 50 ). Firm adhesion and spreading of monocytes on the surface of the endothelium requires functional LFA‐1 and VLA‐4 binding to their receptors ICAM‐1 and VCAM‐1 expressed on activated endothelium ( 50 ).…”