Annual Symposium 2023

SYIS Annual Symposium 2023

The SYIS is thrilled to announce its second SYIS Annual Symposium! After a successful event last year, we are ready to welcome you in Bern for a day full of immunology, and more. The symposium is organized as a pre-congress event to the SSAI Annual Meeting.

Attendees can apply for a Swiss Society for Allergology and Immunology (SSAI) travel grant to fund their travel via this webpage and an EFIS travel grant through the Symposium registration form.

Event at a glance

When: 23 August 2023
Where: Auditorium Ettore Rossi, Inselspital, University of Bern
More info on the event (directions, certificate of attendance) can be found here:

Practical info for participants

Registration deadline: 1 August 2023
Abstract submission deadline: ~~30 June 2023~~ 15 July 2023
Fees
– SYIS/SSAI members: CHF 20
– Non-members: CHF 40*

*Take the chance to become a member via this page. You will be able to join the Symposium with a reduced fee and have additional benefits.

Program

Time	Session
9.30	Opening address
9.45	Prof. Dr. Salomé LeibundGut-Landmann – “Immunosurveillance of fungal commensalism“
10.30	Prof. Dr. Francesca Ronchi – “Diet-microbiota effect on the gut-brain axis“
11.00	Coffee break
11.30	Oral presentations from selected abstracts (4x, 15 min)
12.30	Lunch
13.30	Prof. Dr. Ping-Chih Ho – “Mitochondrial dynamics guides T cell anti-tumor responses“
14.15	Flash talks from selected abstracts (10x, 2 min)
14.45	Poster session
15.45	Coffee break
16.15	Dr. Florian Mair – “Disentangling human tumor-unique immune alterations from non-malignant tissue inflammation“
16.45	Panel discussion on Career Development with Prof. Arnaud Didierlaurent, Prof. Nicole Joller, Dr. Chiara Pazzagli and Dr. Maria Vono
17.45	Closing address
18.00	Apéro

Confirmed speakers

Keynote talks

Prof. Dr. Salome LeibundGut-Landmann, University of Zurich

Immunosurveillance of fungal commensalism
Tissue homeostasis is a central aspect of mammalian physiology. Commensal microbes colonizing the barrier tissues can be seen as an integral part of homeostatic circuits that contribute to the maintenance of tissue homeostasis by protecting the barrier tissues against injury and infection. Given their own pathogenic potential to overgrow, invade and damage the host epithelia, commensal microbes themselves need to be strictly controlled. My lab studies the fungal community of commensal microbes and how these organisms are kept in check by the immune system. Using experimental mouse models of colonization, we aim at dissecting the homeostatic immune mechanisms against Candida albicans and Malassezia, to major fungal commensals of the mucosa and skin, respectively. In my talk I will provide an overview of IL-17-mediated antifungal immune mechanisms in both of these tissue environments. In addition, I will discuss recent discoveries of the fungal determinants driving these protective responses at the interface with the host. Mutual adaptations between the fungal commensals and the immune system ensure continuous homeostasis and prevention of disease.

Prof. Dr. Ping-Chih Ho, University of Lausanne

Mitochondrial dynamics guides T cell anti-tumor responses
Metabolic challenges in tumors attenuate metabolic fitness and tumoricidal activity of tumor-infiltrating T lymphocytes (TILs). Although emerging studies uncovered that metabolic insufficiency compromises TIL anti-tumor activity by interfering signaling cascades and transcriptional program, it remains unclear how TILs adjust metabolic program in response to sustained metabolic stress and whether durable metabolic challenges could reinforce commitment of T cell exhaustion. Since adjusting mitochondrial dynamics is a critical process to tackle metabolic challenges, Dr. Ping-Chinh Ho will discuss how mitochondrial dynamics in TILs is compromised and the contribution of this deregulated process on reinforcing T cell exhaustion.

Short talks

Prof. Dr. Francesca Ronchi, Charité – University Medicine Berlin

Diet-microbiota effect on the gut-brain axis
The central nervous system (CNS) and the intestine communicate via peripheral nervous structures, the immune system and via intestinal microbial products and metabolites, building a bidirectional network called gut-microbiota-brain (GMB) axis. The microbiota is highly influenced by the dietary habits of the host. Ketogenic diet (KD) not only changes the microbiota composition but ameliorates conditions in several metabolic and neurologic diseases. However, the mechanisms behind the effect of this dietary intervention are not well understood. We aim to unravel the effects of KD on the function of gut microbiota and the host metabolism, the immune system and the CNS under healthy conditions. To study the microbiota, we performed 16S rRNA sequencing and metatranscriptomics on intestinal bacteria of mice colonized with a diverse and undefined microbiota (specific-pathogen free, SPF) or with a gnotobiotic moderately diverse microbiota and fed purified KD or control diet. KD changed the Firmicutes/Bacteroidetes ratio and the metabolism of Clostridia families. To investigate the effect of KD on the CNS in a microbiota-dependent and -independent way, we analyzed the brain performing spatial transcriptomics in germ-free and SPF mice fed KD and control diet. In the brain, KD induced, in a microbiota-dependent manner, the upregulation of genes involved in neuronal cell communication and development, myelinization, and metabolic processes within specific areas, such as the hypothalamus, thalamus, amygdala and the hippocampus. We are currently investigating the effect of KD and microbiota on the host at the single cell level, via single nuclei RNA seq, in the affected brain areas and via flow-cytometry to identify the role of the immune system in our model. Behavioral tests will be performed to address the CNS functions in the different experimental conditions.
Our experiments provide important findings to unravel the mechanisms behind the effects of KD on the host via the microbiota

Dr. Florian Mair, ETH Zurich

Disentangling human tumor-unique immune alterations from non-malignant tissue inflammation
Anti-tumor immunotherapies have achieved remarkable successes in the treatment of cancer, but major challenges remain. An inherent weakness of current treatment approaches is that the therapeutically targeted pathways are not restricted to tumours, but are also found in other tissue microenvironments.
Despite great efforts to define inflammatory processes in the tumour microenvironment, our understanding of tumour-unique immune alterations is limited by a knowledge gap regarding the immune cell function in inflamed human tissues. Here, in an effort to identify such tumour-enriched immune alterations, we used complementary single-cell analysis approaches to interrogate the immune infiltrate in human head and neck squamous cell carcinomas and site-matched non-malignant, inflamed tissues.
Our analysis revealed a large overlap in the composition and phenotype of immune cells in tumour and inflamed tissues. Computational analysis identified tumour-enriched immune cell interactions, one of which yields a large population of regulatory T cells (Tregs) that is highly enriched in the tumour and uniquely identified among all haematopoietically-derived cells in blood and tissue by co-expression of ICOS and IL-1 receptor type 1 (IL-1R1). We provide evidence that these intratumoural IL-1R1⁺ Treg cells had responded to antigen recently and demonstrate that they are clonally expanded with superior suppressive function compared with IL-1R1^– Treg cells.
Overall, our work highlights how combining several single-cell techniques with subsequent validation experiments can provide critical new insight into the function of immune cells in human tissues.

More details will be published soon.

We thank EFIS for sponsoring travel grants

Recipients of the EFIS travel grant:

Verena Lentsch
Valeria Oliva
Matthias Rath
Mariolina Brunoo
Maria Cruz Cobo
Manal Bel Imam
Luca Schlotheuber
Ioana Sandu
Ignacio Gonzalez Perez
Flurina Boehi
Flavia Fico
Burak Kizil
Anna Estrada Brull
Annika Hausmann