ArticleImmunology2026
Immune Consequences of Metabolic Syndrome and Its Treatment: A Cytokine Perspective.
Article in Immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Metabolic Syndrome (MetS) is characterized by a set of clinical conditions that elevate cardiovascular risk and may interfere in several pathways of the immune system, as well as the medications used for its treatment. The aim of this study was to evaluate antigen-specific and polyclonal cellular immune responses in patients with MetS. Thirty-two participants were divided into three groups: individuals with MetS in use of medication for metabolic conditions (MST), individuals with MetS without treatment (MS), and healthy donors (HD). Blood samples were collected, and peripheral blood mononuclear cells were obtained and stimulated in vitro with peptide pools to evaluate antigen-specific and polyclonal responses. Supernatants were collected for quantification of interleukin-2 (IL-2), interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α), and interleukin-10 (IL-10). Intragroup comparisons revealed that the MS group showed a more diverse cytokine production compared to the other groups after antigen-specific stimulation, that could represent a more vigorous immune activation. The comparison of groups revealed that the MST group produced lower levels of IL-2 and IL-10 than HD and lower levels of TNF-α than the MS group after polyclonal stimulation. This attenuated response in the MST group may have multiple causes, such as the inhibitory effects of hyperglycemia on cytokines production and/or the use of medication for metabolic conditions that may exhibit anti-inflammatory effects. Therefore, the MS group demonstrated a broader cytokine production profile after antigen-specific stimulation, whereas the MST group exhibited quantitatively lower cytokine production in response to polyclonal stimulation. The implications of these findings require further investigation.
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