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Adipokines, Inflammation, and Metabolic Diseases · Journal article
Journal of Food Innovation, Nutrition, and Environmental Sciences · September 7, 2026
Raises a question worth testing. It does not answer one.
This is a narrative review that synthesizes existing knowledge on immune-cell-mediated inflammation in obesity and its relationship to inflammaging. It identifies gaps in evidence and calls for human studies and targeted therapeutic approaches, but does not present new empirical findings or test hypotheses.
Narrative review. Obese individuals and the mechanistic role of immune cells in obesity-related metaflammation; general discussion without specific cohorts studied..
Macrophage accumulation and activation, especially interaction with T cells, shows consistent evidence linking to adipose metabolic dysfunction Evidence for roles of other immune cells (B cells, NK cells, NKT cells, neutrophils, eosinophils, mast cells) is more variable Metaflammation and inflammaging share immune dysregulation and inflammatory signaling but differ in primary triggers: nutrient excess and metabolic stress versus biological ageing and cellular damage
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Clinicians should recognize that immune-targeted therapies in obesity require careful balance to avoid impairing protective immunity and host defense. The review highlights that current evidence supports macrophage-T cell targeting more strongly than other immune modulation strategies, pending human clinical translation.
A narrative review synthesizing mechanistic knowledge of immune-cell roles in obesity-related inflammation; raises questions for future research rather than presenting new empirical evidence or testing interventions.
As stated by the source record.
Clinicians should recognize that immune-targeted therapies in obesity require careful balance to avoid impairing protective immunity and host defense. The review highlights that current evidence supports macrophage-T cell targeting more strongly than other immune modulation strategies, pending human clinical translation.
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.
What is missing. This record has no reported figures. That is a gap in the analysis, not a judgement about the study.
Chronic low-grade metabolic inflammation (metaflammation) is a hallmark of obesity and plays a role in adipose-tissue dysfunction, insulin resistance and metabolic comorbidities. Recruitment and activation of immune cells play a key role in this process, but their role is dependent on adipose tissue depot, disease stage and cellular phenotype. This review article focuses on the innate and adaptive immune cells such as macrophages, T cells, B cells, natural killer (NK) cells, natural killer T (NKT) cells, neutrophils, eosinophils and mast cells and their role in the inflammation associated with obesity. The evidence linking macrophage accumulation and activation, especially the interaction with T cells, to adipose metabolic dysfunction is more consistent, although evidence for other immune cells is more variable. Additionally, the link between metaflammation and inflammaging is also discussed. While they have common traits of immune dysregulation and inflammatory signaling, metaflammation is mostly triggered by nutrient excess and metabolic stress, and inflammaging by biological ageing and underlying cellular and molecular damage. There is a need for clinical translation of therapeutic targeting of inflammatory pathways, although this is not straightforward as these pathways are essential for host defense and tissue homeostasis. Human studies, understanding immune-cell heterogeneity and developing targeted approaches to inhibit pathological inflammation without affecting protective immune responses should be the focus of future research.
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