The IUIS Webinar Series was established at the beginning of 2020 as an online education programme with the aim to provide individuals from all around the world the opportunity to gain comprehensive knowledge on the latest COVID-19 research developments without the need of travelling in these uncertain times. This first series was a tremendous success:
internationally-acclaimed speakers shared their insights and latest research results on COVID-19-related topics in 20 webinars that welcomed more than 8,800 scientists from 86 countries.
For its second series, IUIS, in partnership with Immunopaedia, will broaden the scope to cover a variety of hot topics in
immunological research such as Autoimmunity, Infectious Diseases and Allergology.
Hyperinflammation: hemophagocytic lymphohistiocytosis and macrophage activation syndrome
Date: May 24, 2021
Time: 3 PM CET
The webinar will cover clinical presentations and laboratory features of hyper-inflammation with a focus on hemophagocytic lymphohistiocytosis (HLH) and macrophage activation syndrome (MAS). Pathogenic mechanisms and the involvement of cytokine networks in different forms of hyper-inflammation will be discussed. The webinar will also cover conventional therapeutic approaches, as well as novel targeted therapies
Speaker: Fabrizio De Benedetti
Dr De Benedetti, a physician scientist, has obtained his MD, Board certification in Pediatrics and PhD at the University of Pavia, Italy. His clinical activity has focused on the diagnosis and treatment of children with rheumatic diseases. Since 2010, he is Head of the Division of Rheumatology at Ospedale Pediatrico Bambino Gesù, Rome. His research activity focuses on the role of inflammatory cytokines. His research led to the identification of novel biomarkers of disease activity and prognosis in several pediatric rheumatic diseases and the identification of novel therapeutic targets he designed and led several international clinical trials of novel biologicals.
Moderator: Hanne Ostergaard
Dr. Ostergaard completed her PhD in Immunology at the University of California, Los Angeles (UCLA) where she worked on the mechanisms of CD8 T cell mediated killing. She then moved to The Salk Institute for her postdoctoral studies where she worked on the tyrosine phosphatase CD45 and identified one of its substrates to be the tyrosine kinase Lck. She then moved to the University of Alberta where she has been since 1991. Her research centers on mechanistic studies that examine the cell biology of how these CD8 cytotoxic T cells migrate and function.
On demand Webinars
Please find below the on demand Webinars from the IUIS Webinar Series “Immunology without Borders”. This Series was started in February of 2021 and includes a wide arrays of topics.
Claudia Mauri: Regulatory B cells and gut-microbiota: an intricate acting balance in autoimmunity
Regulatory B cells (Bregs) are immunosuppressive cells that contribute to the maintenance of immunological tolerance (Mauri and Bosma, 2012). Bregs suppress a variety of immune pathologies including autoimmune diseases through the produc- tion of interleukin (IL)-10, IL-35, and transforming growth factor beta 1 (TGFb1) (Mauri and Bosma, 2012). They inhibit the expan- sion of pathogenic T cells and other pro-inflammatory lymphocytes, and promote regulatory T cell (Treg) differentiation (Carter et al., 2011; Rosser et al., 2014). Toll-like receptor (TLR) agonists, including lipopolysaccharide (TLR4) and CpG oligo-deoxynucleotides (TLR9), in combination with low grade levels of inflammatory cytokines, for example IFNa and/or IL-1b and IL-6, induce IL-10-producing Breg differentiation (Lampropoulou et al., 2008; Menon et al., 2016; Rosser et al., 2014). The strength of these inflammatory signals is key in determining whether immature B cells develop into Bregs or into mature B cells and antibody-producing plasma cells (Menon et al., 2016). We have recently shown that low-grade inflammatory sig- nals that drive the differentiation of immature B cells into Bregs are provided in the gut-associated lymphoid tissue (GALT) as a result of the interaction between the gut microbiota and the innate immune system (Rosser et al., 2014). Mice depleted of endogenous bacteria following administration of broad-spectrum antibiotics do not develop arthritis or Bregs, suggesting an intricate relationship between microbiota, inflammation, and Breg differentiation (Rosser et al., 2014). The question of whether inflammatory signals produced in response to the microbiota control Breg development alone or whether microbial factors also play a direct role remains unanswered. We will discuss how butyrate supplementation suppresses arthritis in a Breg-dependent manner by increasing the level of the serotonin-derived metabolite 5-Hydroxyindole-3-acetic acid (5-HIAA), which activates the aryl-hydrocarbon receptor (AhR), a newly discovered transcriptional marker for Breg function.
Qian Zhang: Inborn errors of type I IFN immunity in patients with life-threatening COVID-19
Clinical outcome upon infection with SARS-CoV-2 ranges from silent infection to lethal COVID-19. We identified autosomal-recessive or autosomal-dominant deficiencies of genes in the type I IFN circuit in 23 patients (3.5%) 17 to 77 years of age. We showed that inborn errors of TLR3- and IRF7- dependent type I IFN immunity can underlie life-threatening COVID-19 pneumonia in patients with no prior severe infection.
Antonio Lanzavecchia: Immunology taught by Plasmodium falciparum
Plasmodium falciparum uses multiple strategies to evade the human immune response. While infection is established by a small number of sporozoites that are largely ignored by the immune system, the abundant blood stage parasites use multiple and polymorphic variant surface antigens to avoid clearance and subvert the immune response. From volunteers immunized with irradiated sporozoites, we identified a family of potent neutralizing antibodies that bind to multiple sites of the CSP protein and represent a new tool for prophylaxis and for vaccine design. Using a systematic search for antibodies that bind broadly to infected erythrocytes, we discovered, in 10% of malaria-exposed individuals, a new class of antibodies generated by insertions of genomic DNA encoding human inhibitory receptors (LAIR1 or LILRB1) into antibody genes (at the V-DJ junction or in the switch region). LAIR1- and LILRB1-containing antibodies bind to different families of parasite RIFINs and opsonize infected erythrocytes. These findings demonstrate that the parasite uses multiple RIFINs to target inhibitory receptors as part of its evasion strategy. They also illustrate a new mechanism of diversification based on the insertion of host receptors into immunoglobulin genes, leading to the production of receptor-based antibodies, with implications for antibody and B cell engineering.
Eric Vivier: Harnessing innate immunity in cancer therapy and beyond
New therapies that promote antitumor immunity have been recently developed. Most of these immunomodulatory approaches have focused on enhancing T-cell responses. Although these therapies have led to unprecedented successes, only a minority of cancer patients benefit from them, highlighting the need to identify new cells and molecules that could be exploited in the next generation of immunotherapy. Given the crucial role of innate immune responses in immunity, harnessing these responses opens up new possibilities for long-lasting, multilayered tumor control. We will present innovative anti-tumor therapies based on the manipulation of the innate immune system. In addition, given the urgent need for effective treatments for pneumonia in patients with COVID-19, the elucidation of the immune responses that occur during the course of COVID-19 could lead to the repurposing of approved immunomodulatory drugs and candidate drugs that have already been tested in clinical trials. Along this line, we will present our results indicating the association of COVID-19 inflammation with activation of the C5a–C5aR1 axis.
Pamela Ohashi: Immunoregulation and the tumor microenvironment
Although PD-1 blockade has transformed cancer treatment, a deeper understanding of tumor immunobiology and inhibitory mechanisms are needed to take immunotherapy to the next level. This webinar will cover topics including the cell types that express key B7 family members and their receptors including PD-L1, B7-H3, B7-H4 and PD-1 and discuss whether these findings align with the traditional views for what is going on in the tumor microenvironment. In addition, it will cover unexpected immunoregulatory mechanisms that we have found focussing on innate lymphoid cells.
This webinar is supported by: Thermo Fisher Scientific
The production of this webinar is supported by Thermo Fisher Scientific. Thermo Fisher Scientific has had no influence on the content, and full editorial control remains the sole responsibility of IUIS.
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