D1.415 - Regulatory T‑Cell Deficiency and NF‑κB/IL‑1β Activation in Dilated Cardiomyopathy

Dilated cardiomyopathy (DCM) is associated with immune dysregulation contributing to myocardial remodeling. Regulatory T‑cells (Treg), defined by Foxp3 expression, play a central role in maintaining immune tolerance. Impaired Treg function may facilitate pro‑inflammatory activation through NF‑κB signaling and cytokine release, including IL‑1β.

Myocardial tissue samples from 12 patients with DCM and a control group of 10 individuals without cardiac pathology were analyzed. Gene expression levels of Foxp3, NF‑κB, and IL‑1β were quantified using quantitative polymerase chain reaction (qPCR). Descriptive statistics were calculated, and intergroup differences were assessed (p‑values reported).

Foxp3 expression was significantly reduced in DCM patients (mean 0.36 ± 0.05; p=0.00001), indicating a marked deficiency of Treg‑associated transcriptional activity compared to controls. NF‑κB expression was elevated (mean 3.56 ± 0.63; p=0.0003), consistent with activation of pro‑inflammatory transcriptional pathways. IL‑1β levels were also increased (mean 16.77 ± 8.81; p=0.0436), reflecting enhanced cytokine production. The combined pattern of Foxp3 downregulation with NF‑κB and IL‑1β upregulation suggests a coordinated shift from immunoregulatory to pro‑inflammatory programming in DCM.

DCM is characterized by deficient Treg activity (↓Foxp3) accompanied by NF‑κB activation and IL‑1β elevation, supporting impaired immunoregulation and enhanced inflammation. This immune signature highlights potential therapeutic targets including restoring Treg function and modulating NF‑κB/IL‑1β pathways which may attenuate disease progression.