Adipose tissue specific CCL18 associates with cardiometabolic diseases in non-obese individuals implicating CD4+ T cells
An erratum to this article was published (Cardiovasc Diabetol, 30 Aug 2023 ↗)
Authors' conclusion
We suggest that in T2D and CVD, increased production of CCL18 recruits and activates CD4+ T cells to secrete IFN-γ and TGF-β. This, in turn, promotes adipocyte lipolysis - a possible risk factor for cardiometabolic diseases.
Study context
- Population
- Non-obese individuals, population-based cohort; 17 cytokines measured in white adipose tissue (WAT) and circulation, immune cells phenotyped by 13-color flow cytometry
- Participants
- 17 / 16 / 18 / 19
- Exposure
- Non-obese T2D, cardiovascular disease (CVD) and T2D + CVD vs non-obese healthy controls
- Healthyn = 17reference
- T2Dn = 16
- CVDn = 18
- T2D + CVDn = 19
- Outcome
- WAT inflammatory status: CCL18 and CD4+ T cells
Methodological detailspopulation-based cohort, in vitro mechanistic experiments
- Population-based cohort
- In vitro mechanistic experiments
Main finding
As reported in the abstract
- CCL18 and CD4+ T cells significantly upregulated in CVD, T2D and CVD + T2D vs healthy controls
- WAT CCL18 secretion correlated with WAT CD4+ T cell amounts; these cells highly expressed CCL18 receptors
Observational data: associations, not effects.
Further findings
In vitro adipocyte lipolysis (glycerol release)
- Direct rCCL18 addition to mature adipocytes did not alter lipolysis
- Conditioned media (CM) from CCL18-treated T cells increased adipocyte glycerol release
- IFN-γ and TGF-β secretion significantly induced in CM from CCL18-treated T cells
- Blocking IFN-γ and TGF-β in CM prevented CM-induced upregulation of adipocyte lipolysis
Original publication
Adipose tissue specific CCL18 associates with cardiometabolic diseases in non-obese individuals implicating CD4+ T cells. Cardiovasc Diabetol. Published 12 April 2023. doi:10.
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