Loading
Obesity / Natural Cytotoxicity Triggering Receptor 1 · Journal article
Immunology Letters · August 10, 2026
Early or partial results. Treat as a signal, not a conclusion.
This is an ex vivo mechanistic study examining leptin's modulation of NK cell signaling in normal-weight and obese donors. The work identifies weight- and sex-dependent differences in ERK1/2, p38, and mTOR phosphorylation, and correlates reduced signaling with impaired granzyme B and IFN-γ responses in obesity, but provides no clinical endpoint or therapeutic actionability.
Cross-sectional ex vivo mechanistic study. Normal-weight and obese adults; stratified by sex. Setting, age range, BMI criteria, and recruitment details not specified in abstract.. Intervention: Leptin exposure, including high-concentration condition (50 nM). Compared with: Normal-weight donors; baseline NK cell phenotype without leptin stimulation.
Obesity associated with reduced circulating NK cell frequencies, particularly in women High-concentration leptin (50 nM) enhanced IFN-γ production in NK cells from normal-weight individuals but induced suppressive response in obese donors NK cells from obese individuals showed reduced phosphorylation of ERK1/2 and p38 following leptin stimulation
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
This mechanistic work suggests leptin resistance in NK cells from obese individuals may contribute to immunological dysfunction in obesity. However, the lack of sample size reporting, clinical outcomes, and validation limits immediate clinical application; findings are hypothesis-generating rather than practice-informing.
In vitro mechanistic study of leptin signaling in NK cells from obese and normal-weight donors; no clinical outcome, uncontrolled design, and findings require validation in larger populations.
As stated by the source record.
Quoted from the source exactly as published.
This mechanistic work suggests leptin resistance in NK cells from obese individuals may contribute to immunological dysfunction in obesity. However, the lack of sample size reporting, clinical outcomes, and validation limits immediate clinical application; findings are hypothesis-generating rather than practice-informing.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
Obesity is characterized by chronic inflammation and sustained hyperleptinemia, conditions known to disrupt immune homeostasis. Natural killer (NK) cells are particularly sensitive to metabolic cues, and obese individuals frequently display impaired NK cell activity. Here, we investigated how leptin modulates NK cell frequency, activation, effector function, and intracellular signaling in normal-weight (NW) and obese (OB) adults. Obesity was associated with reduced frequencies of circulating NK cells, particularly among women, along with decreased expression of the activating receptors CD16 and NKp46. Upon leptin exposure, NK cells from obese donors exhibited impaired effector function, characterized by reduced granzyme B intensity and diminished IFN-γ production. Leptin further modulated these responses in a weight-dependent manner: whereas high-concentration leptin (50 nM) enhanced IFN-γ production in NK cells from normal-weight individuals, it induced a suppressive response in cells from obese donors. At the signaling level, NK cells from obese individuals showed reduced phosphorylation of ERK1/2 and p38 following leptin stimulation, which correlated with impaired cytotoxic and cytokine responses. In contrast, mTOR phosphorylation was intrinsically reduced in NK cells from obese donors, independent of leptin exposure. Sex-stratified analyses revealed higher mTOR activation and granzyme B expression in NK cells from lean men compared to lean women under high leptin conditions, whereas leptin-mediated suppression of IFN-γ was more pronounced in men across both NW and OB groups. Together, these findings suggest that leptin exerts divergent effects on NK cells depending on metabolic and sex-related context, contributing to the functional impairment observed in obesity.
Taken from the source record, never inferred. Follow any of these and new work involving them reaches your briefing.