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Isolation of Adipose Tissue Immune Cells
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Altered NK cell function in obese healthy humans.

Tobias Laue1, Christiane D Wrann2, Birgit Hoffmann-Castendiek3

  • 1Institute for Functional and Applied Anatomy, Hannover Medical School, Hannover, Germany ; Centre for Pediatrics and Adolescent Medicine, Hannover Medical School, Hannover, Germany.

BMC Obesity
|July 29, 2015
PubMed
Summary

Obesity is linked to cancer, but mechanisms are unclear. This study found that natural killer (NK) cells from obese individuals exhibit functional deficits and altered responses to leptin compared to lean individuals.

Keywords:
CD107aImmunityLeptinNatural killer (NK) cellsOb-RObesityTRAIL

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Area of Science:

  • Immunology
  • Cancer Biology
  • Metabolic Disorders

Background:

  • Obesity is a significant risk factor for various cancers, yet the underlying mechanisms remain poorly understood.
  • Leptin, a hormone primarily produced by adipocytes, regulates energy balance and possesses immunomodulatory effects, particularly on natural killer (NK) cells.
  • This study investigates the functional impact of leptin on NK cells in obese versus lean individuals.

Purpose of the Study:

  • To compare the function of NK cells from obese and lean healthy individuals.
  • To investigate the effect of leptin stimulation on NK cell phenotype and activity.
  • To explore the signaling pathways and functional outcomes of leptin interaction with NK cells.

Main Methods:

  • Classification of 20 healthy individuals into normal weight (<25 kg/m²) and obese (>30 kg/m²) groups based on BMI.
  • Isolation of peripheral blood mononuclear cells (PBMCs) and assessment of NK cell markers (CD107a, CD178, TRAIL) via flow cytometry.
  • Analysis of JAK2 phosphorylation (Western Blotting), NK-cell-tumor-cell conjugate formation, and cytokine production (IFN-γ) following in vitro leptin stimulation.

Main Results:

  • Obese individuals had significantly lower numbers of CD3(+)CD56(+) NK cells compared to lean individuals.
  • NK cells from obese subjects showed reduced JAK2 phosphorylation and lower levels of the functional marker TRAIL.
  • In vitro leptin stimulation enhanced interferon-γ production in NK cells from normal-weight subjects, but long-term stimulation did not affect NK cell proliferation.

Conclusions:

  • Natural killer (NK) cells from obese individuals display functional impairments.
  • Obesity alters NK cell responses to leptin stimulation, suggesting a potential link between obesity, immune dysfunction, and cancer susceptibility.