Cell intrinsic TGF-beta1 regulation of B cells.

International audienceTGF-beta family cytokines play multiple roles in immune responses. TGF-beta1-null mice suffer from multi-organ infiltration that leads to their premature death. T cells play a central role in the TGF-beta1 phenotype, as deficiency of TGF-beta1 only in T cells reproduces the lethal phenotype. Although it is known that TGF-beta1 controls B cells isotype switch and homeostasis, the source responsible for this control has not been characterized. Because of the major role that T cells play in regulating B cell responses, we addressed the T cell dependency of the TGF-beta1 control of B cells. The analysis of T cell-deficient, TGF-beta1 knockout mice and the production of chimeras in which B but not T cells lacked TGF-beta1 allowed us to show that B cells are controlled in part by cell autonomous production of TGF-beta1

Cell Intrinsic TGF-β1 Regulation of B Cells

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Developing technologically enhanced mathematics pedagogical content knowledge in initial teacher education

© Springer Nature Switzerland AG 2019. Nowadays perspectives on mathematics education argue for student-centred maths teaching that enables students to engage into learning activities and to play an active role in learning. Information and communication technological evolution provides teachers with an ever-increasing diversity of digital and smart tools that may successfully promote students’ deep engagement with the learning tasks. However, mathematics teachers need to learn how to integrate mathematics pedagogical content knowledge with technological knowledge so that they can develop technologically enhanced mathematics pedagogical content knowledge (TEMPCK). TEMPCK is required for teachers to select the best technological tool to teach a given content in the best way to a certain group of students in a specific social and cultural context. Initial mathematics teacher education has a key responsibility on this issue as it is expected to form updated teachers, able to effectively cope with the technological challenges of the moment as well as with the unanticipated challenges of future technology advancements. This chapter presents a few attempts of prospective mathematics teachers to use digital tools to teach different mathematics topics to secondary school students. Suggestions are made to increase the smartness of the learning environments used by the prospective teachers.(undefined)info:eu-repo/semantics/publishedVersio

Priming of Protective Anti-Listeria monocytogenes Memory CD8+ T Cells Requires a Functional SecA2 Secretion System ▿

The SecA2 auxiliary secretion system of Gram-positive bacteria promotes the export of virulence proteins essential for colonization of the host in the case of both Mycobacterium tuberculosis and Listeria monocytogenes, two intracellular bacteria causing diseases in humans. We and others have demonstrated that this secretion system is also linked to the onset of long-term CD8+ T cell-mediated protective immunity in mice. In the case of L. monocytogenes, expression of SecA2 inside the cytosol of infected cells correlates with the generation of CCL3-secreting memory CD8+ T cells that are required for protection against secondary challenge with wild-type (wt) L. monocytogenes. Since the SecA2 ATPase is well conserved among Gram-positive pathogenic bacteria, we hypothesized that SecA2 itself bears evolutionarily conserved motifs recognized by cytosolic pattern recognition receptors, leading to signaling events promoting the differentiation of CCL3+ memory CD8+ T cells. To test this possibility, we generated a stable L. monocytogenes chromosomal mutant that expressed a SecA2 ATPase bearing a mutated nucleotide binding site (NBS). Similarly to a SecA2 deletion mutant, the NBS mutant exhibited rough colonies, a bacterial chaining phenotype, an impaired protein secretion profile, and in vivo virulence in comparison to wt L. monocytogenes. Importantly, mice immunized with the SecA2 NBS mutant were not protected against secondary infection with wt L. monocytogenes and did not develop CCL3+ memory CD8+ T cells. NBS mutant and wt SecA2 proteins were expressed to comparable extents by bacteria, suggesting that SecA2 itself is unlikely to promote the induction of these cells. Rather, one or several of the SecA2 substrate proteins released inside the cytosol of infected cells may be involved