Sum of i^2: Interdisciplinary immunology

By lorenz adlung

Illustration by Anne-Gaëlle Goubet for SYIS

The sum of many parts
I love immunology. Studying the immune system in all its complexity is thrilling and fascinating. It is challenging, but every day, I learn something new: Seeing things from a different angle. It is my firm belief that immunology is a research branch that offers, but also requires, particularly versatile perspectives.

In my TEDx talk “Let’s talk science – it saves lives”, I argue why medical research in general needs to involve experts from multiple fields. Immunology represents a paradigm in this case. The fact that data generation per se is no longer a limitation (as outlined in my previous SYIS blog post) is not unique to immunology. The technology for high-throughput and/or high-quality data does exist. Computational experts are needed for data analysis, and mathematical modelling is applied across all fields of study ranging from developmental biology to cancer research. What is it that makes immunology unique?

Figure 1: Number of publications mentioning “interdisciplinary immunology” on PubMed per year since 1973.

The immune system is involved in almost every physiological process from cognition to digestion. When I asked the scientific community on Twitter to name any disease the immune system is not involved with, there were hardly any suggestions… Do you have any? The immune system awaits us behind every corner of life sciences. Since you are reading these lines, you probably share my enthusiasm and curiosity about immunology to some extent. From outside our precious scientific community, I see a trend to involve experts from other disciplines within the last decade. In 2011, the Nobel Prize in Physiology or Medicine was awarded to Bruce A. Beutler, Jules A. Hoffmann and Ralph M. Steinman for their fundamental discoveries concerning innate and adaptive immunity (link). In the years after, the number of publications on “interdisciplinary immunology” started rising (Fig. 1). Of course, there are plenty potential covariates – reasons that could possibly explain the rise. However nowadays, experts with different backgrounds are working all together in immunology: Computer scientists, physician scientists, molecular and cell biologists, microbiologists and virologists, biochemists, mathematicians, and physicists. This variety is present in my own group, too. Even though we are just six people working in “systems immunology”, our backgrounds include: molecular and cell biology, mathematics, computer science and medicine. Fun fact: None of us can be considered a “classical immunologist” by training. It is the sum of our backgrounds that builds something bigger. What will be emerging from our joint quest is truly interdisciplinary immunology research [1].

Janus head when facing current challenges
Looking ahead, to sustain these developments of more interdisciplinary immunology research, we need to incorporate concepts into the curricula at universities. Interdisciplinary immunology training programs already exist for instance at the University of Iowa, Tufts, or Stanford Medicine. Education must be broad and inclusive to give students from all backgrounds a chance to understand central concepts in immunology. Because in turn we need those students helping us with their approaches, such as from engineering, to understand the cellular and the humoral immune response as what they are: a complex system. A system as intricate as the immune system can only be understood with various measures in combination by involving multiple fields of study.
Looking back (c.f. Fig. 1), you may argue that the previous rise of “interdisciplinary” publications is true in general, also for other fields, not only for immunology. But immunology not only requires input of experts from many different fields. The output of immunology research translates to different disciplines of clinical research, too. A prime example is immunotherapy. The Nobel Prize in Physiology or Medicine 2018 jointly awarded to James P. Allison and Tasuku Honjo highlights the role of immunotherapy for cancer research (link). Lately, immunotherapy also yielded promising pre-clinical results in the context of metabolic disorders (Science Translational Medicine). Thus, immunology requires interdisciplinary input, but therefore also provides interdisciplinary output.
Yes, immunology can be quite complex. An aspect hard to understand in immunology is plasticity and its role in health and disease, as nicely outlined in a previous blog post by Jeremy Yeoh. Once we understand such phenomena, benefits can emerge that are valuable even outside of our field (e.g. for transplantation medicine, developmental biology, etc). We must face both sides: the interdisciplinary nature of our research and its wide implications beyond immunology [2]. The COVID-19 pandemic showed that interdisciplinary immunology research is demanded and key to our success. We are not there yet (Nature Immunology Editorial). There are challenges ahead of us. But together, we have the highest chances to succeed. Another reason why I love immunology.

[1] The quote “The whole is greater than the sum of the parts” is attributed to the Ancient Greek philosopher Aristotle (384–322 BC).
[2] Janus is an ancient Italian diety (namesake of the month January) depicted with two faces, looking forward and backward, here rather representing interdisciplinary input and output of immunology research.

The SYIS does not guarantee the accuracy of the content published in this blog. The content does not necessarily reflect the opinion or views of the SYIS.

Gut Neuroimmunity – Teamwork makes the dream work  

By Jeremy Yeoh

Illustration by Anne-Gaëlle Goubet for SYIS

One unpleasant aspect of the upcoming summer is the rise of undesirable insects (no offence to entomologists). The advent of the insect season brings upon us much suffering – mainly in the form of itchy and sometimes painful bites, causing pain and inflammation in the form of a red welt. Well, as the saying goes ‘no pain, no gain’ – this itchy bump is a coordinated effort by both the nervous and immune systems actively reacting to danger to protect us (by avoiding and preventing pathogen’s entry). While some people would think of pain as an annoying side effect, the nervous system can play a bigger role in influencing our immunity than one might think and possibly vice versa.

Brief History of NeuroImmunity

Neuron-mediated pain and immune-mediated inflammation have been thought to be linked since around 2000 years ago. Further experiments in the 1800s and 1900s corroborated this hypothesis, where denervation in the skin led to a decrease in inflammation. Given the advances in biochemistry in the 60s, these principles and mechanisms behind this interaction was starting to be understood with the discovery of neuronal mediators of inflammation in the form of signaling molecules. More recently in the early 21st century, the ‘inflammatory reflex’ showed the vagus nerve playing an active role in suppressing the production of a key inflammatory cytokine, tumor necrosis factor (TNF), in splenic macrophages during peripheral inflammation. Interestingly, this phenomenon has been linked also with the elevated inflammatory state in obesity. One area of interest recently for neuroimmunity has been the enteric nervous system (ENS), which surrounds our gut from our stomach to our anus. This so-called ‘second brain’ has two-thirds the number of neurons of a cat, can operate autonomously and can live with or without communication with the parasympathetic and sympathetic nervous systems. As such, the field of neuroimmunity has largely been concentrated on this area.

Deciphering the Code – How two biological systems with different functions speak to each other

As of today, we have observed both seemingly interconnected systems speaking the same language – with immune-associated receptors (PRRs) being expressed on neurons and neuronal-associated receptors (neuropeptides) on a medley of innate and adaptive immune cells. Of recent interest are gut-resident innate immune cells like macrophages, mast cells and innate lymphoid cells (ILCs). During homeostasis, muscularis macrophages (MM) lying close to the enteric nerves can modulate muscular contraction and receive in return sustenance in the form of macrophage colony stimulating factor (M-CSF) by neurons. Other innate immune cells are also involved with neuronal signaling when things start going wrong. During visceral pain, mast cells (most well known for their involvement in allergies) can degranulate upon receiving neuropeptides, where it can drive the sensitization of sensory neurons. These neuronal nociceptors can sense pain through messengers (histamines, prostanoids, inflammatory cytokines) produced by immune cells, indicating a coordinated effort of our body in informing our brain that something is wrong and to take corrective measures.

‘Two’s company, but three’s a crowd’ – Gut Microbiota adding a new facet of regulation to health A major part of the gut that we have not addressed here is our many little friends living with us – our microbiota. It is increasingly clear that our microbiota has widespread effects on our body and to nobody’s surprise, it can also tune and regulate neuroimmunity. Gut immunity is widely reported to be evolutionarily adapted to co-exist with our commensal flora, with neurons in close proximity with the epithelium, microbiota, and immune cells (Fig 1).

Figure 1: Illustration showing the cellular organization of neuroimmune interactions in the gut. Figure taken from Margolis et al.

Neurons and immune cells can interact with the microbiota in a variety of ways (PAMPs, metabolites, neurotransmitters). There is also some evidence that suggests that neurons can also regulate the microbiome composition. This triangle of co-regulation between the microbiota, immune cells and neurons is tightly regulated, where any dysregulated compartment will affect the others. Consequently, it makes it a gut-wrenching challenge to determine the origins of certain pathologies in the intestines, where Jacobson et al. further posits that these systems should be interrogated as one integrated system to obtain a better understanding of the overall picture.

NeuroImmunity and Disease

Coming back to pain and immunity, certain diseases have been linked to a dysregulated neuro-immune circuitry, mainly Irritable Bowel Syndrome (IBS) and Inflammatory Bowel Disease (IBD). These diseases come with debilitating visceral hypersensitivity and abdominal pain, severely impacting quality of life. Due to the intense crosstalk between the microbiota, immune system and nervous system mentioned above, it is still unclear which component is responsible for/initiated this dysregulation. Nevertheless, one of the identified major drivers of disease flares in IBS is stress, suggesting that it can be initiated by cues from the brain (via stress hormones).  

Exciting Horizons for Treating Inflammatory Diseases

With an increasing understanding of the mechanisms behind neuroimmunity, bioelectric medicine is starting to be implemented for the treatment of certain autoimmune/inflammatory diseases (i.e rheumatoid arthritis). This is mainly done through stimulation of the vagus nerve to manipulate the ‘inflammatory reflex’ mentioned above, via implantation of a small device (pill-sized) into your neck to stimulate the vagus nerve (Fig 2).

Figure 2: Illustration showing how the mechanism of bioelectric-based therapeutics. Figure taken from Koopman et al.  

While the idea of electrocuting yourself might be a bit shocking, the dose of current released by the implant are minimal as the nerve fibers are extremely sensitive. Currently, this method is still a burgeoning field with a ‘one size fits all’ approach; however researchers/engineers are working on ways to innervate specific organs of interest via targeting specific nerve fibers. Bioelectric medicine has therapeutic potential as a complementary approach to traditional treatments, which often have strong side effects. One of the end goals for bioelectric medicine is the development of a ‘closed loop therapy’, where the device can adapt and decipher the signals between cells and respond appropriately – and this can only be done with more insights on these crosstalks in neuroimmunity. If you find this field of two interconnected disciplines interesting, I highly recommend these reviews (Pain & Inflammation, Crosstalk of Microbiota/Neurons/Immunity, Bioelectric Medicine, Immunology and Psychiatry) that comprehensively illustrate our current understanding in the field.

Main Takeaways

  1. Complex crosstalk exists between the nervous system and the immune system, that can be tuned by the microbiota in certain organs.
  2. The study of neurology and immunity as one integrated system in certain diseases may give us a better pathological understanding.
  3. Future of bioelectric medicine and neuromodulatory drugs may ameliorate inflammatory diseases.

The SYIS does not guarantee the accuracy of the content published in this blog. The content does not necessarily reflect the opinion or views of the SYIS.

Plasticity: An Identity Crisis

By Jeremy Yeoh

Illustration by Anne-Gaëlle Goubet for SYIS

Have you ever felt like you don’t really fit in a box that was meant to describe you? Do you feel like both a Pisces and a Scorpio at the same time? To make our lives simpler, humans tend to categorize things into neat groups, whether it be ourselves, other humans or immune cells. However, in immunology, classification and categorization of cell identities are getting increasingly difficult as the numbers of different cell types that have been identified are getting out of hand with the advent of new technologies. This is getting even more problematic by the concept of plasticity in biology, creating a professional organizer’s worst nightmare.

Some Immune Cells Are Plastic! (Not The Environmentally Unfriendly Type of Plastic)
The general idea in cell biology is that you start from an omnipotent stem cell, gradually differentiating and gaining different functions until it reaches a terminal permanent state that has defined roles within a system. This is termed as lineage stability. However, what we observe is not that straightforward. Plasticity in immunity is in principle defined as the ability of cells to acquire changes in phenotype and/or function in response to a dynamic environment. This would suggest that plastic cells generally exist more on a spectrum with fluid identities rather than on a binary basis – a landscape of cells instead of defined non-changing personas, complicating the attempted categorization of these cells into tidy little boxes.

It seems that the closer we head towards specialized pathogen-specific immunity, the more we see this phenomenon of plasticity – starting from macrophages and dendritic cells (the bridges to adaptive immunity) to the specific immune arm of the adaptive immune system, lymphocytes. As the immune system gets more specialized and specific, plasticity allows for a degree of flexibility in responding to the situation. For the purpose of keeping it simple, here we will focus the discussion on immune plasticity on that of the celebrities (in my opinion) – T cells. These lymphocytes have multiple intermediate phenotypes which were previously thought to be polarized subsets.

Understanding Plasticity
To discuss plasticity in broader terms, a discussion of the state of the field by Mills et al. in EMBO nicely illustrates cellular differentiation and plasticity as balls within a groove. The most relevant type of plasticity in immunity is trans differentiation, where cells acquire new cell identity without reversion to an immature state. To properly define plasticity, Mills et al. suggested that certain concepts need to be clarified:

  1. Is it trans differentiation or re-differentiation?
  2. If the cell divides during the transition to acquire new functions, is it still trans differentiation?
  3. Are these cells acquiring new phenotypes or are they a completely new subset of cells?
  4. How many new features does it have to adopt before defining as being a different cell type?

While some of these questions remain for the most part unanswered due to the technical limitations of observing dynamic processes in- vivo, immunologists have continued to move forward with categorizing new subsets of T cells and deciphering the mechanisms behind these intermediate phenotypes. A review by DuPage and Bluestone in 2016 comprehensively summarizes the different mechanisms of T cell plasticity as we understand it so far, where immune plasticity generally depends on the milieu of the stimulus present (strength and composition of cytokine/TCR   stimulus).

An illustration of different types of plasticities and unanswered questions in a tissue differentiation landscape envisioned by Waddington. Grooves indicating the tissue environment, whereas bottom of the grooves indicating terminal differentiation. Figure taken from Mills et al. (2019).

Plasticity – Beneficial or Detrimental?
Now, is plasticity just a remnant of evolution, where its vestigial function remains to be selected out? How crucial is it to the daily functioning of our immune system? Turns out, these cells are just as functional as their single-minded counterparts depending on the situation – raising the question of ‘if we only had these plastic cells, wouldn’t we be able to cope with every situation appropriately?’ The keyword here is ‘appropriate’, since our immune system, while extremely impressive, also has its flaws. To paraphrase a certain superhero: ‘with great flexibility comes frequent miscommunication’. T cell plasticity is also involved in a medley of immune-driven diseases – ranging from Th1/Th17 cells in multiple sclerosis to Th17/Tregs in colorectal cancer.

The regulatory triad of regulating cell plasticity. Figure adapted from DuPage and Bluestone (2016). Created with

Nevertheless, having flexible cells makes extraordinary evolutionary sense considering the breadth and evasiveness of the pathogens our body is exposed to. As pathogens are able to transition from one microenvironmental niche to another (i.e extracellular to intracellular in certain parasites), our immune system also needs to be able to effectively transition from one effector response to another to not lose ground in this race. Therefore, it is still extremely beneficial to maintain this flexibility afforded to us by plasticity. In the end, similar to many other facets in immunology, balance and appropriate regulation of this flexibility has to be maintained to keep the system running smoothly. To that extent, to understand how to manipulate this inherent flexibility in these cells, the mechanisms and concepts behind plasticity has been a topic of interest over the past two decades and is still under research.

The Way Forward
One of the ways we can discover new phenotypes is through in-silico predictions with mathematical modelling based of previous experimental data, followed by in-vivo validation using fate-mapping techniques and new single cell technologies such as scRNA-sequencing and mass cytometry (CyTOF) available for large scale immunophenotyping. So, we are getting there! While it can be slightly messy with the current state of cell phenotypes, as long as the phenotype of any cell associated with high plasticity is properly defined, it would still allow us to define its relevance in a disease regardless of its stability as a cell sublineage. A small dose of organized chaos has never hurt anybody.

Main Takeaways:

  1. Immune plasticity may complicate categorization of cells and questions the concept of immune cell identity.
  2. With the rise of single cell analysis techniques, large scale immunophenotyping would allow us to better understand these plastic populations by giving insights into the immune landscape as a complex whole instead of a biased attempt at simplifying immune populations.
  3. T cell plasticity can be exploited and harnessed for future therapies in different diseases.

The SYIS does not guarantee the accuracy of the content published in this blog. The content does not necessarily reflect the opinion or views of the SYIS.

Social networks within the immune system

By lorenz adlung

Illustration by Anne-Gaëlle Goubet for SYIS

Everything is connected!
Immune cells communicate with each other thereby forming intricate interaction networks like the one on the right from our work published 2019 in Cell. With recent advances in technology, we understand more about functional interdependencies between immune cellular subsets. Immune cells reside in various tissues and circulate through the bloodstream as they are forming an interconnected web. The availability of fate-mapping mice, multiplexed cellular assays, as well as tissue profiling with unprecedented molecular and spatial resolution allow for an in-depth characterisation of social networks within the immune system.

In 2018, I speculated about integrating all this information, e.g. the transcriptional and the proteomic layer. Meanwhile, there are methods that combine several high-throughput techniques. So in theory, we can measure everything together. But how much of everything do we need to know to learn something new? The team led by Professor Bernd Bodenmiller of the University of Zurich and ETH Zurich has shown that the answer to that question depends on the tissue of interest. The team was dealing with imaging mass cytometry data – in simple terms: pointillistic pictures (see below) of tissue sections, containing information on both, RNA and protein.

The preprint from the Bodenmiller lab introduces an algorithm for intelligent experimental design planning such measurements.

Unlimited data
It becomes clear that data itself is no longer a limitation. It is rather our ineptitude to conceptualise ideas, which hampers the transformation (“translation”) of data into hypotheses that can be experimentally tested. I want to highlight this aspect with another example from social networks within the immune system, namely intercellular communication. Shortly after the advent of single-cell RNA-sequencing protocols, algorithms were introduced to computationally infer cellular interactions. They come in different flavours (such as “CellPhoneDB”, or “NicheNet”, to name just two) and in essence, they do all the same: they construct a bipartite graph, which is a table with two columns. The first column contains the sender cell and molecule. An example would be a pro-inflammatory macrophage expressing Il1b. The second column contains the receiver cell and molecule. The corresponding example would be a neutrophil expressing Il1r1. If the query dataset contains both sender and receiver cells and molecules, the entries are put in the same row of the bipartite graph table, and a connection can be made.

It’s a match!
Those inferred connections have to be critically evaluated for several reasons.

  1. It’s sparse: Single-cell RNA-sequencing data is like good Swiss cheese – full of holes. Transcriptome-wide coverage particularly for lowly expressed genes cannot be taken for granted. A way to deal with sparse data is to impute missing values. But imputed values can introduce false positives. So you assume there is a transcript whereas in reality there is none.
  2. It’s merely RNA: Just because there are transcripts in the data does not mean that the corresponding proteins are correctly produced and transported to the cell surface for actual interactions. Translation or post-translational modifications can be erroneous.
  3. Partners are unclear: For IL-1β, the receptor is well known. But since it is a complex including also IL1-R3, presence of IL-1β and IL1-R1 alone will not suffice for an interaction. There are other examples for which interacting pairs of ligand and receptor are not yet clearly defined. The triggering receptor expressed on myeloid cells 2 (Trem2) is such an example – it is a lipid receptor, but the exact molecules, which are sensed, remain elusive.
  4. Proximity unknown: Sender cells secrete molecules that can be bound by receptor molecules on the surface of receiver cells. However, such an interaction only occurs if they are in proximity allowing a physical interaction of both entities prior to eventual depletion.
    From my experience, the detection of “significant” cellular interactions with the methods mentioned above depends on data quality and data processing. If I fail to identify specific subsets of immune cells within my data, the chance is very high that the algorithms miss interactions among those subsets. The reason is that specific (and therefore rare) interactions are “diluted” below the detection limit in the coarser (and therefore bigger) immune populations.

Keep it simple!
Accordingly, an ultimate proof of inferred interactions is in vitro. After all those new-gen technologies, we are going back to old-school co-cultivation experiments. Take macrophages and/or neutrophils from conditional knock-out mice, put them together and test whether cell communication is abrogated as expected! I believe that such straightforward experiments are a precondition to probe the existence and functional relevance of social networks within the immune system.

Post scriptum
Data-driven predictions go hand in hand with experimental validation. If you share my network perception of the immune system and beyond, you may want to contribute to our special issue of Cells in the context of the gastro-intestinal tract:

The SYIS does not guarantee the accuracy of the content published in this blog. The content does not necessarily reflect the opinion or views of the SYIS.

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16 December Seminar (on Zoom only) – Two talks by the Astrophysicist and Astrobiologist Daniel Angerhausen

daniel angerhausen, ethz, the explainables, zurich

Dr. Daniel Angerhausen is an Astrophysicist and Astrobiologist at the Institute for Particle Physics and Astrophysics (IPA) at the Physics Department of ETH Zurich, where he leads the Project Office and the Science Team Lead for the LIFE (Large Interferometer for Exoplanets) space  mission. The former NASA and Center for Space and Habitability fellow is also founder and CEO of the Science and Tech Communication start-up ‘Explainables’, a diverse team of highly qualified young communicators from all over the globe. On his search for planets around other stars Daniel already flew six missions on the NASA airborne telescope SOFIA. Daniel is also mentor and science committee member of NASA Frontier Development Lab, an Artificial Intelligence/Machine Learning incubator tackling challenges in various fields of space sciences in collaboration with industry stakeholders such as Google Cloud, Nvidia or IBM. Daniel plays Sepaktakraw, an artistic footvolleyball game and competed several times at World Championships in South East Asia.  

Science talk – Aliens, Exoplanets and Astrobiology 

In my presentation I will give a non-expert introduction to the field of Astrobiology and in particular the science of extrasolar planets, planets orbiting stars outside our Solar System.
I will describe my various projects in this emerging field using the largest ground based telescopes, the ‘flying telescope’ SOFIA (Stratospheric Observatory for Infrared Astronomy) and the Kepler and Hubble space telescopes.
I will explain how these methods will – for the first time in history – enable us to systematically search for life in space in the next two decades.

soft-skills talk – Authentic personal Branding in Academia (in a nutshell)

A branding strategy can be a crucial step in winning grants, building a scientific reputation and advancing your career. Networking at all career levels and between disciplines is a key skill to establish professional relationships within academia or the job market in the industry.
How do I establish an authentic personal brand? Which are my options for sharing information? How do I build and maintain relationships in my community or with potential future employers in the industry? I will give a short introduction to some key concepts that will help to develop a personal brand and to exercise networking skills.

02 December Seminar – The divergent effects of CD4 T cells and insights on entrepreneurship in science

Carolyn King, UniBasel, basel

Science talk

Activated CD4 T cells have the remarkable ability to differentiate into many different types of effector subsets. This diversification is required for the generation of specialized and pathogen appropriate T cell responses, as well as long-lived and protective memory T cells. Although CD4 memory T cells are clearly important to control various infections (i.e. tuberculosis), vaccines targeting the induction of polyfunctional memory cells have had only limited success. In some cases, CD4 memory T cells can also induce host detrimental effects, for example during chronic viral infection or after organ transplantation. We hypothesize that these divergent effects are dependent on heterogeneity within the CD4 memory T cell compartment, the plasticity of these cells following recall, and their localization relative to other cells or environmental signals. Thus, a major goal of our work is to elucidate the specific factors regulating CD4 memory T cell diversification and their relationship to host immunity. We are using several infection models as well as complementary microscopy approaches to assess the dynamics and flexibility of T cell differentiation.

Carla benichou, Baselaunch, basel

career talk

Very early on during my biology undergraduate studies, I had two somewhat contradictory Have you ever thought about creating your own biotech start-up? Early stage starts up are in demand in Switzerland, as early phase financing increased by 43% in 2020 and life science sector set new records as the investment in biotech grew by 31.3%. This talk will interest you if you want to learn more about entrepreneurship in science and the available support to help you building the next cutting edge therapeutics company. Martyna and Carla will introduce you to BaseLaunch accelerator, its selection process and the program benefits. After this session, you will have a better view on when there is start-up potential, how to go about starting a venture and why the field of start-ups can be an attractive career path. They will go through the real life cases of immunology start-ups to illustrate this.

18 November Seminar – The dynamics of antiviral immunity and insights from a science journalist

Spatial-temporal dynamics of antiviral immunity across stromal cell-underpinned niches

Natalia Pikor, IKSSG, St. Gallen

Science talk

Efficient priming and effector functions of adaptive immune responses require the optimal positioning and interaction of lymphocytes in their environment. The topology of immune cell interactions is steered by stromal cells, non-hematopoietic cells that provide niche factors to direct the homing, sustenance and interaction of immune cells. The stromal – immune cell interaction landscape has thus far been best described in secondary lymphoid organs. Here, we explore the role for stromal cells to orchestrate efficient antiviral immunity in the CNS following neurotropic coronavirus infection.

Science journalist – neither in nor out

florian fisch, horizonte magazin

career talk

Very early on during my biology undergraduate studies, I had two somewhat contradictory goals: I wanted to do real research and communicate science to a wider public. Would both become possible? Today I can say that I was lucky enough to be able to do both, even if both turned out differently than I initially thought. In my presentation, I will explain why journalism is not the same as explaining research results. And I will give you an insight into how we produce the Swiss research magazine Horizons.

04 November Seminar – Antigen discovery and CyTOF technology

Antigen discovery for development of personalized cancer immunotherapy.

Michal Bassani, University of Lausanne


Cancer immunotherapy has revolutionized the clinical outcome of patients. At the Department of Oncology at the CHUV, several personalized cancer vaccines and adoptive T cells based therapy phase I trials have been launched and a few more are under development. These exploratory therapies are based on the activation of the immune system to recognize and eliminate tumors based on recognition of mutated neoantigens presented specifically on the surface of cancer cells. Mutations are often private to each patient, hence comprehensive target discovery approaches have been put in place, including whole exome sequencing, transcriptomics and mass spectrometry based immunopeptidomics analyses. The computation analyses of such sensitive data must be completed within a define timeframe required for the manufacturing of the treatment products. In my presentation, I will describe our computational and experimental pipeline for antigen discovery that we have developed for these trials.

An introduction to CyTOF technology for high-multiplex cell suspension and imaging applications

Anne-Sophie Thomas-Claudepierre, fluidigm

career TALK

The next-generation mass cytometer, CyTOF XT, redefines high parameter cytometry with advances in automation, throughput, time to results and total cost of ownership. Built to simplify the design and execution of deep cell profiling studies, CyTOF XT™ standardizes sample analysis with reproducible workflows and automation to accelerate novel therapeutic development and improve human health.
With Imaging Mass Cytometry™ (IMC™), also based on established CyTOF® technology, researchers have access to the world’s first and most proven approach to high-multiplex imaging and single cell protein analysis. With the possibility of analyzing the tissue microenvironment with single cell resolution, researchers can now generate novel research hypotheses with fewer samples in one scan. Enjoy flexible panel design without panel or antibody limitations or concern about antibody order or label assignment. Eliminate autofluorescence, create compact easy to work with data files and avoid timely and costly cyclic tests.