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DÖRING LAB – CHEMOKINE-(RECEPTOR) GUIDED CELL CROSSTALK

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DÖRING LAB

DÖRING LAB

We focus on chemokine(-receptor) crosstalk with leukocytes and vascular cells in cardiovascular diseases.

Projects:

Roles of CXCL12 and its receptors CXCR4 and ACKR3 in chronic arterial vascular inflammation.
ChemR23-mediated vascular immune responses in cardiovascular disease
Function of chemokine receptor CCR8 in guiding anti-inflammatory immune cell-crosstalk in atherosclerosis

Yvonne Döring

LATEST NEWS FROM THE LAB

Targeting immune cell recruitment in atherosclerosis

25 Apr 2024 | News | Publication

NATURE REVIEWS CARDIOLOGY 2024 ➤ IPEK scientists discuss here the latest research on receptor–ligand pairs and interactors that regulate leukocyte influx into the inflamed artery wall.

New signalling pathway uncovered, shedding fresh light on atherosclerosis

22 Jan 2024 | News | Publication

NATURE CARDIOV. RES. 2024 ➤ IPEK scientists from the Weber and Döring Labs have found new mechanisms involved in the development of inflammatory cardiovascular diseases.

IPEK at the ESC Congress 2023

31 Aug 2023 | News | Award | Conference

CONFERENCE HIGHLIGHT ➤ Under this year‘s slogan „Joining forces to protect the heart“ the ESC Congress took place in Amsterdam and was a great success.

CCR8-Tregs (NCR)

Recently, we identified a novel interaction of CCR8 expressed on CD4+ T cells and CCL17 in driving atherosclerosis. Specifically, we showed that CCR8-CCL17 interaction restraint Treg suppressive function via CCL3 release binding to CCR1 on Tregs. Conversely, blockade of CCR8 decreased CCL3 levels and attenuated atherosclerotic lesion development concomitant with an increase in Treg numbers (Döring et al., 2024, Nat Cardiov Res).

CCR8-ILC2

Importantly, CCR8 is also highly expressed on ILC2s. Therefore, we are examining the role of CCR8 on ILC2s in chronic vascular inflammation. In particular, we are interested in (adipose-)tissue crosstalk of ILC2s via chemokines and their receptors in atherosclerosis.

CXCL13-CXCR5 dyad, CXCR4 and B cells in atherosclerosis.

We recently described a proatherogenic role of the CXCL13-CXCR5 dyad in atherosclerosis, an effect that is likely attributable to its impact on B1 cells and their IgM production.

Similarly, we could show that expression of the chemokine receptor CXCR4 on B1 cells controls IgM titers and thereby mediated atheroprotection underlining the importance of B1 cell–derived IgM in atheroprotection.

Kral et al. Frontiers Immunology 2023

ACKR3 and Dysfunctional adipose tissue

Dysfunctional adipose tissue may contribute to the pathology of several metabolic diseases. Hence, we explored the role of ACKR3 in adipocyte-specific knockouts of Ackr3 in ApoE-deficient mice in order to determine its impact on lipid levels under hyperlipidemic conditions. Adipocyte-specific deletion of Ackr3 results in reduced AT triglyceride and cholesterol content in ApoE-deficient mice, which coincides with increased PPAR-γ and Angptl4 expression. The role of adipocyte ACKR3 in lipid handling seems to be tissue-specific as hepatocyte ACKR3 deficiency did not demonstrate comparable effects.