Research in Teacher Education: Volume 9, No.2, Novermber 2019

The Research in Teacher Education publication is published twice a year by the School of Education and Communities, University of East London, Water Lane, London E15 4LZ. The periodical offers a forum for informed debate and discussion on all aspects of teacher education. The publication showcases work from the teacher education teams at the School of Education and Communities and the wider teacher education community in the UK. The definition of ‘research’, in its broadest sense includes any gathering of data, information and ‘facts’ designed to advance knowledge. While nurturing and publicising the creative talent within teacher education the periodical seeks to stimulate, provoke and extend discussion and debate with other professionals associated with this field. In addition to contributions from the team of teacher educators at the School, each edition of Research in Teacher Education will publish research findings, book reviews and/or opinion pieces from guest writers associated with the School of Education and Communities

Rapid discovery of monoclonal antibodies by microfluidics-enabled FACS of single pathogen-specific antibody-secreting cells

Monoclonal antibodies are increasingly used to prevent and treat viral infections and are pivotal in pandemic response efforts. Antibody-secreting cells (ASCs; plasma cells and plasmablasts) are an excellent source of high-affinity antibodies with therapeutic potential. Current methods to study antigen-specific ASCs either have low throughput, require expensive and labour-intensive screening or are technically demanding and therefore not widely accessible. Here, we present a straightforward technology for the rapid discovery of monoclonal antibodies from ASCs. Our approach combines microfluidic encapsulation of single cells into an antibody capture hydrogel with antigen bait sorting by conventional flow cytometry. With our technology, we screened millions of mouse and human ASCs and obtained anti-SARS-CoV-2 monoclonal antibodies with high affinity (85% of characterised antibodies bound the target). By facilitating access to the underexplored ASC compartment, the approach enables efficient antibody discovery as well as immunological studies into the generation of protective antibodies.This work was supported by the EU Horizon 2020 programme (ERC Advanced Investigator Awards 69566, to F.H. and EU H2020 Marie Skłodowska-Curie Individual Fellowship (MSCA-IF 750772) to T.S.K), the MRC (grant ref. MC_UU_00025/12, to J.E.D.T and TSF ref. MR/T032413/1, to N.J.M, and a scholarship to K.F.), the Medical Research Foundation (MRF-057-0002-RG-THAV-C0798, to J.E.D.T.), the NIHR Cambridge BRC (to J.E.D.T.), NHSBT (grant ref. WPA15-02, to N.J.M), the Wellcome Trust (ISSF ref. 204845/Z/16/Z, to N.J.M), Addenbrooke’s Charitable Trust (grant ref. 900239, to N.J.M), a scholarship from the Cambridge European Trust (to K.F.), a scholarship from St. John’s College Cambridge (to K.F.), a Postdoctoral Research fellowship by Boehringer Ingelheim (to M.I.J.R), an AstraZeneca studentship (to T.N.K), and a Gates Cambridge Scholarship (to G.L.P)

The Glial Differentiation Factor Nuclear Factor One B (Nfib) Induces Differentiation and Inhibits Growth of Glioblastoma.

International audienceThe molecule CD90 is a N-glycosylated, glycophosphatidylinositol anchored cell surface protein, originally described on thymocytes. CD90 has been considered as a surrogate marker for a variety of stem cells and has recently been reported on glioblastoma stem cells. CD90 is also expressed on T lymphocytes, endothelial cells, fibroblasts and neurons. The function of CD90 is not fully elucidated. CD90 has been involved in cell-cell and cell-matrix interactions, in neurite outgrowth, T cell activation and apoptosis. In this study, we confirmed the expression of CD90 on human glioblastoma stem-like cells from serum-free neurosphere cultures. We also observed RNA and protein CD90 expression on primary cell lines from FSC-containing culture (adherent cell lines) and on freshly prepared glioblastoma specimen. In order to study the function of CD90 on glioblastoma cells, we used a silencing strategy to decrease the expression of CD90 on the immortalized U251 cell line. We then compared the viability, the tumor growth and the migration property of the wild-type CD90+ U251 cells and CD90 down-regulated U251 clones. The decrease of CD90 expression did not affect the viability and the tumor growth of U251 cells. In contrast, down-regulation of CD90 mediated the decreased ability of tumor cell migration using both scratch wound healing and boyden chamber migration assays. Experiments are currently on going to test the effect of CD90 expression on tumorigenicity in mice models. In total, this study might lead to better understand the role of CD90 on the pathology in particular in term of tumor migration/invasion of human glioblastoma