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Annual Meeting 2022 - hosted by DANDRITE

11th Nordic EMBL Partnership Meeting 

  • 31 January-2 February 2022 hosted by DANDRITE

11th Nordic EMBL Partnership Meeting

DANDRITE will host the 11th annual meeting of the Nordic EMBL Partnership for Molecular Medicine. The meeting will be held online from 31 January - 2 February 2022.

Attendees include group leaders, postdoctoral and senior researchers, PhD students and coordinators from all of the Nordic EMBL nodes, as well as representatives from EMBL.

The Nordic EMBL Partnership for Molecular Medicine is a major strategic player in Europe’s efforts towards understanding molecular mechanisms of disease. This is made possible by the complementary research expertise of its four nodes: 

  • FIMM (University of Helsinki, Finland)
  • NCMM (University of Oslo, Norway)
  • MIMS (Umeå University, Sweden)
  • DANDRITE (Aarhus University, Denmark)

Monday 31 January

  • Young Investigator's Meeting 
    Time: 16:00 - 18:00 CET   

Tuesday 1 February

  • Young Investigator's Meeting
    Time: 09:00 - 15:00 CET
    Link to online YIM program
  • Steering Group Meeting (online via Zoom)
    Time: 14:30 - 16:30 CET

Wednesday 2 February

Science & Art Competition 2021

It’s time for the 2021 Nordic EMBL Partnership Science & Art competition!

The Nordic EMBL Partnership aims to bring attention to your research by taking a look at the science from a different perspective. We typically look to our research images to convey information. These images also have the power to evoke emotion. We invite you to take a look at the science in the Partnership from an aesthetic angle. What do YOU see?

Submit your unpublished research images, photographs, paintings, drawings or digital design. For inspiration, take a look at images from our previous competitions.  

Please find details about the competion and how to submit your entry at the Nordic EMBL Partnership website HERE

Program committees

Main Meeting Program Committee

  • Barbara Sixt (MIMS)
  • Björn Schröder (MIMS)
  • Esa Pitkänen (FIMM)
  • Helena Kilpinen (FIMM)
  • Sebastian Waszak (NCMM)
  • Marieke Kuijjer (NCMM)
  • Mark Denham (DANDRITE)
  • Sadegh Nabavi (DANDRITE)
  • Poul Nissen (DANDRITE)


YIM Program Committee

  • Alexandra Berg (MIMS)
  • Mirjam Hunziker (MIMS)
  • Iris Lähdeniemi (FIMM)
  • Aino Heikkinen (FIMM)
  • Annikka Polster (NCMM)
  • Meike Sieburg (DANDRITE)
  • Lucie Woloszczuková (DANDRITE)

Keynote Speakers

Keynote Speaker: Johanna Olweus

Attacking cancer with cytotoxic cells genetically armed with therapeutic T-cell receptors

A single infusion of T cells engineered to express Chimeric Antigen Receptors (CARs) targeting the B-cell specific molecule CD19 can cure up to 40% of patients with B-cell malignancies. This has raised high hopes for the development of similarly successful therapies for other cancer types and for patients relapsing from, or ineligible for, CAR19 T cell therapy. However, in spite of major efforts over the last decade, no CAR therapy has yet been approved for non-B cell cancers. An important reason for this is the lack of cell type-specific cell-surface molecules that can be safely targeted. Unlike chimeric antigen receptors, T-cell receptors (TCRs) can recognize intracellular targets presented on MHC molecules, dramatically increasing the number of potential targets. In my talk, I will discuss work from my group whereby healthy donor T-cell repertoires are exploited for the identification of T-cell receptors that recognize either cell-type specific or mutated targets. For example, we recently demonstrated that T cells expressing TCRs specific for peptides from a novel target, the intracellular lymphoid-specific enzyme terminal deoxynucleotidyl transferase (TdT), specifically eliminate primary acute lymphoblastic leukemia (ALL) cells of T- and B-cell origin in vitro and in in vivo. T cells engineered to express such therapeutic TCRs may represent a promising immunotherapy for cancers resisting current therapies.

Keynote Speaker: Mark Denham

Lineage-Restricted Undifferentiated Stem Cells: A Novel Cell Replacement Therapy for Parkinson’s Disease

The differentiation of human pluripotent stem cells (hPSCs) into mesencephalic dopaminergic (mesDA) neurons requires a precise combination of extrinsic factors that recapitulates the in vivo environment and timing. Current methods are capable of generating authentic mesDA neurons after long-term culture in vitro; however, when mesDA progenitors are transplanted in vivo, the resulting mesDA neurons are only minor components of the graft. This low yield hampers the broad use of these cells in the clinic. In this study, we genetically modified pluripotent stem cells to generate a novel type of stem cells called lineage-restricted undifferentiated stem cells (LR-USCs), which robustly generate mesDA neurons. LR-USCs are prevented from differentiating into a broad range of nondopaminergic cell types by knocking out genes that are critical for the specification of cells of alternate lineages. When LR-USCs are differentiated under caudalizing condition, which normally give rise to hindbrain cell types, a large proportion adopt a midbrain identity and develop into authentic mesDA neurons. We show that the mesDA neurons are electrophysiologically active, and due to their higher purity, are capable of restoring motor behavior eight weeks after transplantation into 6-hydroxydopamine (6-OHDA)-lesioned rats. This novel strategy improves the reliability and scalability of mesDA neuron generation for clinical use. 

Keynote Speaker: Andrea Puhar

PIEZO1 acts as an immune sensor for invasive infection

Tight regulation of the immune response is crucial to establish protective immunity against pathogens, while tolerating commensals and avoiding autoimmunity. The detection of microbes is the first step of the immune response to infection. Incoming microorganisms are generally sensed by Pattern Recognition Receptors (PRRs) binding characteristic microbial molecules, which evokes anti-microbial defences through changes in cellular activities and gene expression. Intestinal epithelial cells (IECs) are a barrier to gut microbes and important immune sentinels. Several Gram-negative intestinal pathogens induce secretion of the pro-inflammatory danger signal ATP as a rapid alert response of IECs, resulting in overt intestinal inflammation. However, what triggers ATP secretion during infection is unknown. We show that the formation of plasma membrane ruffles accompanying the invasion of Gram-negative or Gram-positive bacteria is a physical immune signal of infection, which is detected by the mechanosensor PIEZO1. PIEZO1 activation is necessary and sufficient to trigger mechanically-induced ATP secretion via Ca2+ influx and also reprogrammes inflammatory gene expression in IECs. Thus, mechanosensation of invasion-induced plasma membrane distortion initiates immune signaling upon infection, independently of detection of microbial molecules. Given that formation of plasma membrane ruffles is a characteristic and unifying feature of invasive bacteria, our results indicate that, unlike PRRs which are driven by ligand binding, PIEZO1 acts as a mechanically driven immune sensor for invasive infection.