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Related Experiment Videos

Cell adhesion molecules and cutaneous inflammation.

T J Lawley1, Y Kubota

  • 1Department of Dermatology, Emory University School of Medicine, Atlanta, GA 30322.

Seminars in Dermatology
|September 1, 1991
PubMed
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Cell adhesion molecules (CAMs) on leukocytes and endothelial cells mediate cutaneous inflammation by regulating leukocyte infiltration. Inhibiting CAMs can downregulate inflammation, highlighting their critical role in inflammatory processes.

Area of Science:

  • Dermatology
  • Immunology
  • Cell Biology

Background:

  • Cutaneous inflammation involves leukocyte infiltration into skin tissues.
  • Cell-surface proteins on leukocytes, endothelial cells, and keratinocytes are key to inflammation.
  • Leukocyte extravasation requires binding to endothelial cells and traversing the vascular basement membrane.

Purpose of the Study:

  • To examine leukocyte-endothelial cell binding in cutaneous inflammation.
  • To investigate the role of cell adhesion molecules (CAMs) in inflammation.
  • To understand how CAMs regulate the timing and location of inflammation.

Main Methods:

  • Review of literature on leukocyte-endothelial cell interactions.
  • Analysis of the function of cell adhesion molecules (CAMs).

Related Experiment Videos

  • Examination of cytokine-induced regulation of CAM expression.

    • Main Results:

    • Leukocyte-endothelial cell binding is critical for leukocyte extravasation.
    • Specific interactions between CAMs on leukocytes and endothelial cells mediate this binding.
    • Inhibition of CAM binding downregulates inflammation.
    • Proinflammatory cytokines can induce or upregulate CAMs, potentially increasing inflammation.

    Conclusions:

    • Cell adhesion molecules (CAMs) are crucial regulators of cutaneous inflammation.
    • The expression and regulation of CAMs determine the course and specificity of inflammatory responses.
    • Targeting CAMs offers a potential strategy for managing inflammatory conditions.