Innate Immune Recognition

 / Forschung

Innate Immune Recognition

Innate immune cells such as natural killer (NK) cells, innate lymphoid cells (ILCs), and innate-like T cells form the first line of defense against infections and tumors, but can also contribute to chronic inflammation. By studying the molecular mechanisms that regulate their activity, we aim to gain new insights into how these cells distinguish healthy from abnormal cells. We are especially interested in understanding why this recognition occasionally is dysregulated, resulting in increased susceptibility to infections or the development of autoimmune pathology.

Gruppenleitung:

Quirin 
Hammer

Prof. Dr. rer. nat.

Gruppenmitglieder:

No data was found

Our main focus is the functional regulation of NK cells, ILC, and innate-like unconventional T cells. These populations are characterized by rapid responses and represent the first line of defense against infections and developing tumors. However, under certain conditions, they can also contribute to chronic inflammation and autoimmune pathology.

Central aspects of our research are to delineate the molecular signals that enable innate and innate-like lymphocytes to recognize virus-infected cells, and to uncover how they employ their receptors to distinguish between healthy and abnormal cells. To address these questions, we use a broad range of state-of-the-art cellular, in silico, and molecular biology approaches to analyze samples from both healthy donors and patients with ongoing disease.

In parallel to identifying the fundamental signals that initiate and restrict innate and innate-like immune cell activation, we aim to harness these recognition pathways in conditions where they become dysregulated, such as chronic inflammation and autoimmune disorders.

  • Exploring the co-evolution of viruses with innate and innate-like immune cells
  • Characterizing peptide-specific recognition of virus strains by NK cells
  • Defining the molecular recognition profile of innate-like T cells in health in disease
  • Investigating the shared and distinct functional features and molecular identities of innate and innate-like populations

1. Emerging mutation in SARS-CoV-2 facilitates escape from NK cell recognition and associates with enhanced viral fitness

Bilev E, Wild N, Momayyezi P, Sala BM, Sun R, Sandalova T, Marquardt N, Ljunggren HG, Achour A, Hammer Q. PLoS Pathog. 2024.

2. The HLA-B -21 M/T dimorphism associates with disease severity in COVID-19

Strunz B, Momayyezi P, Bilev E, Muvva JR, Chen P, Bister J, Schaffer M, Akber M, Cornillet M; Karolinska KI/K COVID-19 Study Group; Horowitz A, Malmberg KJ, Rooyackers O, Aleman S, Ljunggren HG, Björkström NK, Strålin K, Hammer Q. Genes Immun. 2025.

3. Genetic ablation of adhesion ligands mitigates rejection of allogeneic cellular immunotherapies

Hammer Q, Perica K, Mbofung RM, van Ooijen H, Martin KE, Momayyezi P, Varady E, Pan Y, Jelcic M, Groff B, Abujarour R, Krokeide SZ, Lee T, Williams A, Goodridge JP, Valamehr B, Önfelt B, Sadelain M, Malmberg KJ. Cell Stem Cell. 2024.

4. SARS-CoV-2 Nsp13 encodes for an HLA-E-stabilizing peptide that abrogates inhibition of NKG2A-expressing NK cells

Hammer Q, Dunst J, Christ W, Picarazzi F, Wendorff M, Momayyezi P, Huhn O, Netskar HK, Maleki KT, García M, Sekine T, Sohlberg E, Azzimato V, Aouadi M; Karolinska COVID-19 Study Group; Severe COVID-19 GWAS Group; Degenhardt F, Franke A, Spallotta F, Mori M, Michaëlsson J, Björkström NK, Rückert T, Romagnani C, Horowitz A, Klingström J, Ljunggren HG, Malmberg KJ. Cell Rep. 2022.

5. Peptide-specific recognition of human cytomegalovirus strains controls adaptive natural killer cells

Hammer Q, Rückert T, Borst EM, Dunst J, Haubner A, Durek P, Heinrich F, Gasparoni G, Babic M, Tomic A, Pietra G, Nienen M, Blau IW, Hofmann J, Na IK, Prinz I, Koenecke C, Hemmati P, Babel N, Arnold R, Walter J, Thurley K, Mashreghi MF, Messerle M, Romagnani C. Nat Immunol. 2018.

Prof. Dr. Quirin Hammer

  • Schleswig-Holstein Exzellenz-Chair (Nachwuchsforschungsgruppe)