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MEETING REPORT - The International Congress of Immunology (IUIS) in Cape Town, South Africa- by Nounagnon Romaric Tochoedo

Meeting report by Nounagnon Romaric Tochoedo who was awarded a travel grant by the CFCD
Nounagnon Romaric Tochoedo is PhD student working at A.G Dudziak laboratory at Uniklinik in Erlangen, Germany.

Emmanuelle Charpentier
Understanding of the complex system of CRISPR-Cas
During her presentation she pointed out the mechanism of tracrRNA identification in S. pyrogenes. Next, she described the Cas proteins or complex generation starting from the invading DNA, followed by CRISPR array transcription, pre-crRNA processing and mature crRNA synthesis. We were also honored to understand the CRISPR-Cas9 mechanism. Finally, she demonstrated the importance of CRISPR-Cas technique for both human and mouse studies.

Ellen V. Rothenberg from California Institute of Technology
Molecular Toolkit for emergence of Lymphocytes: Crossing the Lymphomyeloid Bridge
Ellen described T cell development in mice and identified Delta-like Notch ligand on epithelium as key way of Notch signaling important for T cell development. Next, she identified PU.1, a myeloid factor, as a vital molecule for initiation and T cell development timing through the deployment of T-promoting Runx factors.

Eric Vivier
The Divide narrows: NK and Innate Lymphoid Cells
Dr. Vivier really impressed the audience with his talk. He underplayed the mechanism of NK cell adaptation upon pathogen pressure (eg: during HCMV). Next, he described heterogeneity within NK cell at steady state and during infection base on epigenetic footprints. Finally, Dr. Vivier presented ten hallmarks of NK cell tumor immunity.

Param Ramakrishnan
NF-kB c-Rel in dendritic cells is a critical regulator of TLR7-induced skin inflammation
Param’s work revealed the role of c-Rel during TLR7-induced inflammatory genes in DC. When he knocks-out c-Rel in mouse, he observed under TLR7-induced inflammation condition a suppression of pro-inflammatory cytokines (IL-1ß, IL-6, ICAM1 and TNF-a) in DC in contrast to TLR9-induced inflammation condition in which c-Rel deficiency does not affect these cytokines production in DC. His study also highlighted the protective role of c-Rel deficiency in mice suffering from psoriasis. Moreover c-Rel expression is elevated in psoriasis patients. Dr Ramakrishnan finally suggested that targeting c-Rel holds potential to control psoriasis and other TLR7 dependent inflammations.

Max Krummel
The Assembly of Reactive Archetypes of Tumor Immunity based on Dendritic Cells and Star Effector T cells
Dr Krummel’s talk was focused on DC-T cell interaction in tumor microenvironment. He described how type I & II responses contribute both in the tumor regression. Type I (CD8) responses required NK-CD103+cDC1 interaction which leads to cDC1 migration into the draining lymph node (LN). In the LN, migratory cDC1 interact with naïve CD8+ T cell whom response promotes tumor rejection. In contrast, CD11b+cDC2 interact with Treg in periphery and upregulate their migration capacity into the draining lymph node. In there, CD11b+cDC2 initiate activation and differentiation of naïve CD4+ T cell which will infiltrate the tumor and promote the tumor rejection. Dr Krummel has highlighted the complementary role of T cell responses (type I & II) during tumor aggressions.

Roxane Tussiwand
Plasmacytoid dendritic cells; when origin matters
Professor Tussiwand ‘s group investigated the origin and function of plasmacytoid dendritic cells (pDCs). Plasmacytoid dendritic cells function in anti-viral immunity as well as their capacity of type-I IFN production have been fully studied. However, pDCs capacity of antigen presentation as well as their role during auto-immunity and anti-tumor immunity still need more attention. Therefore, her goal was to better describe pDCs and study in detail their role during tumor and autoimmune disease as well as their capacity of antigen presentation. Her work revealed two types of pDCs which she named conventional pDCs coming from lymphoid lineage and pDC-like cells which come from myeloid lineage. Conventional pDC development require Ly6d and Siglec-H while pDC-like cells are cDC2 precursor and require KIf4 for their maturation to cDC2. Conventional pDCs are essentially type I IFN producer while pDC-like cells are able of antigen presentation. Moreover, Tussiwand’s Lab showed that pDC-like derived cDC2 induce CD4 T cell that secrete pro-inflammatory/auto-immune and tissue repair related cytokines (Th17-Th22). In skin, cDC2 development impairment from pDC-like cell results in reduction of homeostatic Th17 cells.

Florent Ginhoux
The Ever-expanding DC Universe: Lineages versus States
Professor Ginhoux gave an interesting talk about DC nomenclature. He demonstrated how single cell era promote expansion of dendritic cell nomenclature and how that provoke much more confusion in the field. Ginhoux proposed then DC development stage based on transcriptional factors expression. His Lab revealed two subsets of pre-DC2 such as CD115+ pre-DC2 which will give rise to CD172a+CD16/32- DC2 (DC2B) and Siglec-H+ pre-DC2 which will give rise to ESAM+DC2 (DC2A). Next, he identified KIf4 and Tcf4 as key transcription factor which govern the switch between these pre-DC2s. His group believes however that SiglecH+ B220+) pDCs develop mainly from lymphoid-progenitors.