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Coexpression of CD58 or CD48 with intercellular adhesion molecule 1 on target cells enhances adhesion of resting NK

Domingo F Barber1, Eric O Long

  • 1Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852-1727, USA.

Journal of Immunology (Baltimore, Md. : 1950)
|December 24, 2002
PubMed

Insights

Resting NK cells adhere to ICAM-1 via LFA-1, a process modulated by cytokines. Adhesion is enhanced by IL-2/IL-15 and strengthened by LFA-3 or CD48, even without cytokines.

Area of Science:

  • Immunology
  • Cell Adhesion
  • Molecular Biology

Background:

  • The beta2 integrin LFA-1 (leukocyte function-associated antigen 1) mediates lymphocyte adhesion to ICAM (intercellular adhesion molecule)-expressing cells.
  • Adhesion strength is regulated by cytokines, chemokines, and T cell receptor (TCR) signaling.

Purpose of the Study:

  • To identify receptor-ligand interactions crucial for resting natural killer (NK) cell adhesion.
  • To investigate the signaling pathways and modulatory effects of cytokines and co-stimulatory molecules on NK cell adhesion.

Main Methods:

  • Utilized Drosophila cells engineered to express specific human NK cell receptor ligands.
  • Assessed resting NK cell adhesion to ICAM-1 alone and in combination with LFA-3 or CD48.
  • Investigated the role of src family kinase and phosphatidylinositol 3-kinase inhibitors.
  • Examined the impact of IL-2 and IL-15 cytokine pulses on NK cell adhesion.

Main Results:

  • ICAM-1 expression alone supported resting NK cell adhesion, sensitive to src kinase and PI3K inhibitors.
  • Cytokine pulses (IL-2 or IL-15) significantly enhanced actin-dependent NK cell adhesion to ICAM-1.
  • Coexpression of LFA-3 (CD58) or CD48 with ICAM-1 induced strong resting NK cell adhesion, independent of cytokines.

Conclusions:

  • LFA-1-mediated adhesion of resting NK cells to ICAM-1 is regulated by intracellular signaling pathways.
  • Cytokines IL-2 and IL-15 enhance NK cell adhesion through actin-dependent mechanisms.
  • Receptors for LFA-3 and CD48 on NK cells act as co-stimulatory molecules, strengthening LFA-1-mediated adhesion to ICAM-1, particularly in the absence of activating cytokines.

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