Brain, behavior, and immunity · 2026
Systematic review on associations of cancer-related fatigue with proinflammatory cytokines: IL-1alpha, IL-1beta, IL-6, TNF-alpha.
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Kim Hee-Ju, Park Soyoun, Yuk Mi-Kyung, Kang Sujin, Chung Su Wol, Abraham Ivo
Аннотация
OBJECTIVES: This systematic review aimed to identify patterns of associations between cancer-related-fatigue and IL-1α, IL-1β, IL-6, and TNF-α in the literature and to examine the influence of major clinical factors (e.g., disease type and treatment type/trajectory) on the association between fatigue and the selected cytokines, and discuss methodological issues.
METHODS: We searched for data in Pubmed, Embase, and the Cochrane library. Inclusion criteria were original studies published since 2000, an exclusively adult sample, the use of a fatigue measure, and any data related to the selected cytokines. Extracted data included participants' characteristics, data-collection time points, measures, molecules, assay methods, and major findings (associations with each target, other associated factors, and cytokine level).
RESULTS: We selected 53 articles: 24 cross-sectional and 29 longitudinal studies. Most frequently studied targets were IL-6 and TNF-α. Findings from cross-sectional studies are mixed and more studies reported a lack of associations (63% for IL-6, 70% for TNF-α; 71% IL-1β). However, longitudinal studies supported the role of IL-6: 67% of studies reported an association of higher IL-6 with more severe fatigue in at least one time point, particularly during and shortly after treatment. Most studies with TNF-α, the IL-1 family, or their receptors (70% TNF; 69% IL-1) reported a lack of association. The most consistent modifying factors were treatment, time elapsed since treatment, age, body-mass index, and depression. We discussed methodological issues regarding participant selection, measurements, and assay methods.
CONCLUSION: This systematic review supported IL-6 as a potential mechanism of fatigue, particularly during or shortly after treatment. Our review suggests that not only treatment target but also time point in treatment trajectory should be considered in developing an intervention for new targets.
METHODS: We searched for data in Pubmed, Embase, and the Cochrane library. Inclusion criteria were original studies published since 2000, an exclusively adult sample, the use of a fatigue measure, and any data related to the selected cytokines. Extracted data included participants' characteristics, data-collection time points, measures, molecules, assay methods, and major findings (associations with each target, other associated factors, and cytokine level).
RESULTS: We selected 53 articles: 24 cross-sectional and 29 longitudinal studies. Most frequently studied targets were IL-6 and TNF-α. Findings from cross-sectional studies are mixed and more studies reported a lack of associations (63% for IL-6, 70% for TNF-α; 71% IL-1β). However, longitudinal studies supported the role of IL-6: 67% of studies reported an association of higher IL-6 with more severe fatigue in at least one time point, particularly during and shortly after treatment. Most studies with TNF-α, the IL-1 family, or their receptors (70% TNF; 69% IL-1) reported a lack of association. The most consistent modifying factors were treatment, time elapsed since treatment, age, body-mass index, and depression. We discussed methodological issues regarding participant selection, measurements, and assay methods.
CONCLUSION: This systematic review supported IL-6 as a potential mechanism of fatigue, particularly during or shortly after treatment. Our review suggests that not only treatment target but also time point in treatment trajectory should be considered in developing an intervention for new targets.