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Min Ae Lee-Kirsch Group

Molecular genetics of autoinflammatory and autoimmune diseases

Portrait Min Ae Lee-Kirsch

Our group focuses on the molecular mechanisms that underlie autoinflammation and autoimmunity and that are caused by perturbations of the type I interferon (IFN) axis. Type I IFNs play a pivotal role in the first line of defense against viral infections. Activation of type I IFN signaling is induced by pattern recognition receptors of the innate immune system which recognize viral nucleic acids. Nucleic acids are, however, also integral components of the host cell. This implies that cells must be equipped with efficient means to avoid inappropriate recognition of self-nucleic acids and to prevent detrimental immune activation. Combining genetics, molecular and cell biology, we aim to dissect disease mechanisms underlying the phenotypic expression of autoinflammation and autoimmunity.

Future Projects and Goals

  • To identify genes causing monogenic and multifactorial autoinflammatory and autoimmune diseases in humans and to unravel their contribution to disease pathogenesis.
  • To understand the role of the innate immune system in mechanisms of immune defense and tolerance.
  • To translate basic science knowledge into clinically relevant concepts.

Methodological and Technical Expertise

  • genetics
  • molecular and cell biology
  • protein biochemistry/recombinant protein expression
  • confocal microscopy
  • flow cytometry
  • disease modeling using iPSCs


Since 2022
Speaker, Dresden site, European Reference Network-RITA

Since 2022
Speaker, Dresden site, CRC/TRR 237 “Nucleic Acid Immunity”

Since 2021
German Centre for Child and Adolescent Health, Principal Investigator

Since 2014
Vice Speaker, University Center for Rare Diseases, TUD

Since 2012
W2 Professor for Molecular Pediatrics, Department of Pediatrics, TUD

Leader, CRU 249 “Defects of the Innate Immune System in Autoinflammation and Autoimmunity”

Fellow in Cardiology and Genetics, Harvard Medical School, Boston

Doctorate: Dr. med., “summa cum laude”, Free University Berlin

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Selected Publications

Wolf C, Brück N, Koss S, Griep C, Kirschfink M, …, Winkler S, Berner R, Latz E, Günther C, Lee-Kirsch MA
Janus kinase inhibition in complement component 1 deficiency
J Allergy Clin Immunol. 146(6):1439–1442 (2020)

Wolf C, Rapp A, Berndt N, Staroske W, Schuster M, Dobrick-Mattheuer M, Kretschmer S, …, Lee-Kirsch MA
RPA and Rad51 constitute a cell intrinsic mechanism to protect the cytosol from self DNA
Nat Commun. 7:11752 (2016)

Günther C, Kind B, Reijns MAM, Berndt N, Martinez-Bueno M, Wolf C, Tüngler V, Chara O, … , Lee-Kirsch MA
Defective removal of ribonucleotides from DNA promotes systemic autoimmunity
J Clin Invest. 125(1)413-424 (2015)

Hasan M, Koch J, Rakheja D, Pattnaik AK, Brugarolas J, Dozmorov I, Levine B, Wakeland EK, Lee-Kirsch MA, Yan N
Trex1 regulates lysosomal biogenesis and interferon-independent activation of antiviral genes
Nat Immunol. 14(1):61-71 (2013)

Lee-Kirsch MA, Gong M, Chowdhury D, Senenko L, Engel K, Lee YA, de Silva U, Bailey SL, Witte T, Vyse TJ, Kere J, Pfeiffer C, Harvey S, Wong A, Koskenmies S, Hummel O, Rohde K, Schmidt RE, Dominiczak AF, Gahr M, Hollis T, Perrino FW, Lieberman J, Hubner N
Mutations in the gene encoding the 3’-5’ DNA exonuclease TREX1 are associated with systemic lupus erythematosus
Nat Genet 39, 1065-1067 (2007)


University Hospital Carl Gustav Carus
Technische Universität Dresden
Fetscherstraße 74
01307 Dresden