Innate nucleic acid sensing

How a cell reacts to nucleic acids.

Every cell carries DNA and RNA that the immune system can read as danger. What follows that reading is our subject: a sustained interferon response, inflammation, a cell committed to a different fate, a genome full of mobile elements held quiet or let loose. We work on both ends of it — type I interferon–driven inflammation and the fundamental biology of retroelement defense — in primary human cells and in mouse models, and we carry both toward therapeutics.

Research

Two arms, one question

Arm 01 — Immunopathology

Type I interferon–driven inflammation

A persistent interferon response reshapes the cells that live through it, and it does so through hundreds of interferon-stimulated genes whose individual functions are largely unknown. We work through that space gene by gene — in primary human cells and in mouse models — to understand how the response turns into immunopathology, and to identify the nodes within it that can be drugged.

Interferon signature
Autoinflammation
Cell fate
Mouse models

Selected publications

Forbes D, Jorgacevic I, et al. — Interferon-α as a precision medicine tool in Sjögren's diseaseLancet Rheumatol 2026 · PubMed
Schumann T, Costas Ramon S, et al. — Deficiency for SAMHD1 activates MDA5 in a cGAS/STING-dependent mannerJ Exp Med 2023 · PubMed

Arm 02 — Fundamental biology

Retroelement defense

LINE-1 and related retroelements make up a large fraction of the human genome and never stop being transcribed entirely. We study how cells hold that activity in check, what escapes, and how the products are recognised by the nucleic acid sensing machinery.

LINE-1
cGAS–STING
Transposon control
Genome stability

Selected publications

Schumann T, Costas Ramon S, et al. — Deficiency for SAMHD1 activates MDA5 in a cGAS/STING-dependent mannerJ Exp Med 2023 · PubMed
Achleitner M, Kleefisch M, et al. — Lack of Trex1 causes systemic autoimmunity despite the presence of antiretroviral drugsJ Immunol 2017 · PubMed

The shared denominator is sensing. Both arms ask the same question from opposite ends — one from what a sustained response leaves behind, the other from the nucleic acid that sets it off. Methods, mouse lines and people move between them.

Across both arms

Therapeutics

Informed by our two research arms, we actively develop immune therapeutics. We identify novel targets and compounds, and test their efficacy in tailored cell culture models, in vivo models and small investigator-initiated clinical trials.

This work runs with academic groups and with industry partners, for whom we have been reliable collaborators since 2018.

Target identification
Compound screening
Cell culture models
In vivo models
Investigator-initiated trials

Selected publications

Prabakaran T, Troldborg A, et al. — A STING antagonist modulating the interaction with STIM1 blocks ER-to-Golgi trafficking and inhibits lupus pathologyEBioMedicine 2021 · PubMed
Haag SM, Gulen MF, et al. — Targeting STING with covalent small-molecule inhibitorsNature 2018 · PubMed

Publications

Complete list, always current

The full bibliography is maintained on PubMed and updates itself as papers appear. The papers named under each research arm above are a selection; everything else is one click away.

Full bibliography on PubMed

People

Two arms, one group

Prof. Dr. rer. nat. habil. Rayk Behrendt Group leader

Interferon-driven inflammation

Dr. Anne v. MäßenhausenSenior postdoc
Dr. Ivana JorgacevicPostdoc
Aref Mayo, M.Sc.PhD student
Melanie Hega, M.Sc.PhD student
Mustafa ÖztürkTechnician

Retroelement defense

Dr. Lina MuhandesPostdoc
Dr. De XiPostdoc
Kilian Leon Kleemann, M.Sc.Bioinformatics
Jonas Dauster, M.Sc.PhD student
Patrick MüllerTechnician

Alumni

Dr. Emilija MarinkovicSenior postdoc, Roers lab
Dr. Santiago Costas-RamonBioNTech
Lukas SydowMiltenyi Biotec

History

How the group got here

2026Interferon-driven immunopathologyMajor publication with the Hunt lab in Edinburgh, in The Lancet Rheumatology.
2026Associate EditorMolecular Therapy Nucleic Acids.
2025ImmunoSensation³Main applicant of the ImmunoSensation³ Cluster of Excellence.
2024Tenured professorshipPremature promotion to tenured Professor (W2) for Nucleic Acid Immunity and Genome Defense, University and University Hospital Bonn.
2023First major paper from the Bonn labInnate immune priming in autoinflammation, in the Journal of Experimental Medicine.
2022ERC Consolidator Grant awarded“EndoRPHIm” starts the retroelement arm of the group.
2022Move to BonnTenure-track professorship (W2) for Nucleic Acid Immunity at the University and University Hospital Bonn.
2021A new class of STING antagonistDeveloped with the Paludan lab.
2020Habilitation“Molecular mechanisms and therapy of nucleic acid-driven inflammation”; Venia Legendi, Medical Faculty, TU Dresden.
2018First STING antagonistIn vivo work behind the discovery of the first STING antagonist, with the Ablasser lab in Lausanne.
2017Aicardi–Goutières Syndrome Research Award
2017Group establishedInstitute for Immunology, TU Dresden.

Funding

Current and past support

Public funding

Deutsche ForschungsgemeinschaftImmunoSensation³ Cluster of Excellence2026–2032
Deutsche ForschungsgemeinschaftEinzelantrag2027–2030
European Research CouncilConsolidator Grant — “EndoRPHIm”2023–2028
Deutsche ForschungsgemeinschaftEinzelantrag2022–2026
Deutsche ForschungsgemeinschaftSFB/TRR 2372018–2030
Deutsche ForschungsgemeinschaftEinzelantrag2017–2021
Else Kröner-Fresenius-StiftungSchlüsselprojekte2016–2019
Fritz Thyssen StiftungMolecular mechanisms of diseases2013–2015

Industry funding

Industry partnersCollaborative drug development projectssince 2018

Contact

Open to enquiries

Address

Department of Nucleic Acid Immunity & Genome Defense
Institute for Clinical Chemistry and Clinical Pharmacology
University Hospital Bonn
Venusberg-Campus 1, Building 12
53127 Bonn, Germany

Email

behrendt@uni-bonn.de

Joining the group

We take PhD students and postdocs with a background in immunology, virology, molecular biology or computational genomics. Write with a CV and a short note on what you want to work on.