European Congress of Immunology – Part 2

It has begun and Vienna is full of these “hipster” backpack/shopping bags.

After an opening ceremony full off classical live music – today was the first full day of scientific presentations. Each day there is one keynote lecture, several symposia and workshops. At any given time two symposia and six workshops run at the same time. Great in terms of the number of scientists that get to present their work, but for the audience this means choosing.

For me Monday was the day of bright sparks! The organisers chose the 24 most exciting abstracts submitted from young carrier scientists, asked them to give presentations and awarding them with the BRIGHT SPARKS OF IMMUNOLOGY award. Here are my personal highlights from these presentations (yes there is a bias towards innate immune talks – but what can I say personal choice!):

  1. Till-Julius Brühl from Mainz, Germany talked about immunosuppressive molecule produced by ticks, with animated ticks running across the slides! Sialostatin L inhibits the secretions of cytokines like IL-1beta and IL-9 by blocking the transcription factor IRF4 in mast cells. With this knowledge Sialostatin L can now be used to treat asthma, where mast cells are hyperactive and produce to many cytokine. Who would have thought – ticks can be helpful!
  2. Andreas Schlitzer from Bonn, Germany presented work on dendritic cell (DC) development. Using single cell sequencing of 500 dendritic cell progenitors – that means he looked which genes were switched on in 500 individual cells – he found that these progenitors are already primed to become certain DC subsets early on. Their fate is set long before the cells enter their final destination tissue indicating a win of nature over nurture. At least in this instance.
  3. Obviously I need to mention our very own Ann-Cathrin Hofer, a PhD student in our lab in Heidelberg – from now on only known as sparkles. Presenting her PhD thesis, Ann-Cathrin talked about regulatory T cells in the liver, underlining the fact that immune cells have varied and specialised functions in different tissues. She highlighted that younger mice have higher numbers of regulatory T cells in the liver, due to the high degree of cell proliferation in the developing organ.
  4. Edward Chu from Australia showed that long non-coding RNAs (lncRNAs) could function as MyD88 dependent TLR-repressors. LncRNA are encoded in the genome, next to or even within protein-encoding genes, but do not contain a message to transcribe a protein. They rather regulate gene expression directly as RNA molecule. Analysing genetic regions known to be linked to a high incidence rate of diabetes (susceptibility loci), Chu demonstrated that a loss of the lncRNA called Apics can increase the levels of proinflammatory cytokines leading to increased disease rates in induced diabetes models. It appears therefore that lncRNA (Apics and likely others) may be safeguards of the immune responses and help protect us from an overactivated immune system that could leads to autoimmunity.
  5. Marion Espeli from Clamart, France described the effect a gain-of-function mutation in CXCR4 has on B cells, mimicking the Whim-Syndrome, in mice. Increased function of CXCR4 leads to enlarged germ centres and more plasma cells. Antigen-specific plasma cells in the bone marrow are however reduced in number,  while the nice is filled with immature plasmablasts underlining a role of CXCR4 in B cell development.
  6. Rebekka Wehner from Dresden, Germany talked about a DC subtype I personally had not heard of before – SlanDCs. These cells typically induce a Th1 response, but in cancer are primed by tumour cells to induce more Th2-like responses leading to a bad prognosis for patients with high numbers of these DCs.
  7. Dhiren Patel from London, Great Britain postulated that neutrophils may actually be the good guys in asthma as depletion of this cell type in an model of asthma leads to even more inflammation (by means of cellular infiltrates, antibodies and cytokines) in the lungs than in normal asthma. It appears that neutrophiles suppress monocytes from entering the lung during asthma and thereby dampen the inflammation to a certain extend. Patel speculated that neutrophils might prime monocytes already during their development in the bone marrow.

More to follow about the other days…


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