Imaginaires basques et cinéma : trois explorations filmiques

Mémoire en recherche-créationCe mémoire de recherche-création propose d’explorer l’imaginaire basque tel qu’il a été représenté au cinéma. Pour ce faire, nous nous attarderons sur trois films afin d’étudier les différentes facettes de cet imaginaire ainsi que ses évolutions. Le premier chapitre portera sur une série réalisée par Orson Welles, Around the World with Orson Welles (1955), plus spécifiquement sur les deux premiers épisodes se déroulant au Pays basque. Nous verrons comment Welles use de sa figure et de da sa mise en scène afin de mythologiser les Basques et partager au monde leur culture alors même que celle-ci est fortement réprimée et censurée sous l’Espagne de Franco. Le deuxième chapitre propose une étude d’Ama Lur (1968) de Nestor Basterretxea et Fernando Larruquert, film dont la forme représente une démarche de retranscription visuelle de la langue basque, et qui fut le premier long-métrage basque réalisé sous la dictature. Enfin, le troisième et dernier chapitre s’attarde sur une analyse de Vacas (1992) de Julio Medem. Nous observerons comment Medem emploie des éléments récurrents de l’imaginaire basque afin de le détourner et porter un regard critique sur celui-ci. En guise de conclusion, nous parlerons brièvement du film de création accompagnant ce travail, Euskara ez dut mintzatzen. Nous reviendrons sur le processus de création de cet essai documentaire ainsi que sur la manière dont le travail théorique de ce mémoire en a influencé les intentions.This research-creation project explores Basque imaginary and its expression in cinema. For this purpose, three films will be studied in order to uncover the various facets of this imaginary and its evolutions. The first chapter will focus on a television mini-series directed by Orson Welles, Around the World with Orson Welles (1955), more specifically the first two episodes, shot in the Basque Country. We will observe how Welles utilizes his persona and his knowledge of ‘mise en scène’ in order to mythologize the Basque people and share their culture across the world at a time when said culture is strongly censored in Spain by Franco’s regime. The second chapter proposes a study of Ama Lur (1968) directed by Nestor Basterretxea and Fernando Larruquert, a film whose style represents an attempt to transcribe the Basque language in visual form and was the first Basque feature film produced under the dictatorship. Finally, the last chapter will analyze Julio Medem’s Vacas (1992). It will focus on how Medem employs recurring elements of the Basque imaginary and hijacks them so as to deconstruct them critically. To conclude, we’ll take a succinct look at the film Euskara ez dut mintzatzen, the creative endeavor accompanying this thesis. We’ll briefly discuss the creative process behind this documentary essay as well as the influence the written, theoretical portion ultimately had on the making of the movie

Secreted IgM Modulates IL-10 Expression in B Cells

IL-10+ B cells are critical for immune homeostasis and restraining immune responses in infection, cancer, and inflammation; however, the signals that govern IL-10+ B cell differentiation are ill-defined. Here we find that IL-10+ B cells expand in mice lacking secreted IgM ((s)IgM–/–) up to 10-fold relative to wildtype (WT) among all major B cell and regulatory B cell subsets. The IL-10+ B cell increase is polyclonal and presents within 24 hours of birth. In WT mice, sIgM is produced prenatally and limits the expansion of IL-10+ B cells. Lack of the high affinity receptor for sIgM, FcμR, in B cells translates into an intermediate IL-10+ B cell phenotype relative to WT or sIgM–/– mice. Our study thus shows that sIgM regulates IL-10 programming in B cells in part via B cell-expressed FcμR, thereby revealing a function of sIgM in regulating immune homeostasis

A Mucosal and Cutaneous Chemokine Ligand for the Lymphocyte Chemoattractant Receptor GPR15

Chemoattractants control lymphocyte recruitment from the blood, contributing to the systemic organization of the immune system. The G protein-linked receptor GPR15 mediates lymphocyte homing to the large intestines and skin. Here we show that the 9 kDa CC-motif containing cationic polypeptide AP57/colon-derived sushi containing domain-2 binding factor (CSBF), encoded by C10orf99 in the human and 2610528A11Rik in the mouse, functions as a chemokine ligand for GPR15 (GPR15L). GPR15L binds GPR15 and attracts GPR15-expressing T cells including lymphocytes in colon-draining lymph nodes and Vγ3+ thymic precursors of dermal epithelial T cells. Patterns of GPR15L expression by epithelial cells in adult mice and humans suggest a homeostatic role for the chemokine in lymphocyte localization to the large intestines, as well as a role in homing to the epidermis during wound healing or inflammation. GPR15L is also significantly expressed in squamous mucosa of the oral cavity and esophagus with still poorly defined regulation. Identification of the chemotactic activity of GPR15L adds to its reported antibacterial and tumor cell growth regulatory functions and suggests the potential of targeting GPR15L–GPR15 interactions for modulation of mucosal and cutaneous inflammation

Chemerin triggers migration of a CD8 T cell subset with natural killer cell functions

The recruitment of cells with effector functions into the tumor microenvironment holds potential for delaying cancer progression. We show that subsets of human CD28-effector CD8 T cells, CCR7- CD45RO+ effector memory, and CCR7- CD45RO- effector memory RA phenotypes, express the chemerin receptor CMKLR1 and bind chemerin via the receptor. CMKLR1-expressing human CD8 effector memory T cells present gene, protein, and cytotoxic features of NK cells. Active chemerin promotes chemotaxis of CMKLR1-expressing CD8 effector memory cells and triggers activation of the α4β1 integrin. In an experimental prostate tumor mouse model, chemerin expression is downregulated in the tumor microenvironment, which is associated with few tumor-infiltrating CD8+ T cells, while forced overexpression of chemerin by mouse prostate cancer cells leads to an accumulation of intra-tumor CD8+ T cells. Furthermore, α4 integrin blockade abrogated the chemerin-dependent recruitment of CD8+ T effector memory cells into implanted prostate tumors in vivo. The results identify a role for chemerin:CMKLR1 in defining a specialized NK-like CD8 T cell, and suggest the use of chemerin-dependent modalities to target effector CMKLR1-expressing T cells to the tumor microenvironment for immunotherapeutic purposes

The role of JAM-C in innate leukocyte migration and the immune response to Leishmania major infection

Leishmaniasis is a parasitic disease transmitted to humans through sand fly bites. Clinical symptoms vary from self-healing cutaneous lesions to death. Cutaneous leishmaniasis is particularly studied in mice inoculated with Leishmania major. In this model, some strains (e.g. C57BL/6) are resistant due to a Th1 immune response promoting parasite killing. Conversely, other strains (e.g. BALB/c) are susceptible due to a nonprotective Th2 response. DCs are professional antigen-presenting cells that educate antigen-specific T cells. Improving the migration of DCs from the site of infection to the lymph nodes, where T cells reside, may improve the T cell response. JAM-C is a vascular adhesion molecule implicated in leukocyte migration in different inflammatory models. We found that JAM-C blockade with antibodies increases vascular permeability and consequently improves the migration of DCs to sites of infection and draining lymph nodes. This increased leukocyte migration boosted the induction of the Th1 response in resistant mice, while in susceptible mice the Th2 response was augmented. This led to disease improvement or exacerbation, respectively. Our results illustrate the key role of a vascular adhesion molecule in controlling leukocyte migration and the subsequent immune events in response to pathogen infections

Recents Works in Tell el-Fara'in, Late Buto (2016-2019)

International audienc

Recents Works in Tell el-Fara'in, Late Buto (2016-2019)

International audienc

Research Letter: Mechanism-based inhibition of HsaD: a C-C bond hydrolase essential for survival of M. tuberculosis in macrophage

M. tuberculosis remains the leading cause of death by a bacterial pathogen worldwide. Increasing prevalence of multidrug resistant organisms means prioritising identification of targets for anti-tuberculars. 2-hydroxy-6-oxo-6-phenylhexa-2,4-dienoate hydrolase (HsaD), part of the cholesterol metabolism operon, is vital for survival within macrophage. The C-C-bond hydrolase, HsaD has a serine protease-like catalytic triad. We tested a range of serine protease and esterase inhibitors for their effects on HsaD activity. As well as providing a potential starting point for drug development, the data provides evidence for the mechanism of C-C bond hydrolysis. This screen also provides a route to initiate development of fragment based inhibitors. This article is protected by copyright. All rights reserved

Blocking Junctional Adhesion Molecule C Enhances Dendritic Cell Migration and Boosts the Immune Responses against Leishmania major

The recruitment of dendritic cells to sites of infections and their migration to lymph nodes is fundamental for antigen processing and presentation to T cells. In the present study, we showed that antibody blockade of junctional adhesion molecule C (JAM-C) on endothelial cells removed JAM-C away from junctions and increased vascular permeability after L. major infection. This has multiple consequences on the output of the immune response. In resistant C57BL/6 and susceptible BALB/c mice, we found higher numbers of innate immune cells migrating from blood to the site of infection. The subsequent migration of dendritic cells (DCs) from the skin to the draining lymph node was also improved, thereby boosting the induction of the adaptive immune response. In C57BL/6 mice, JAM-C blockade after L. major injection led to an enhanced IFN-γ dominated T helper 1 (Th1) response with reduced skin lesions and parasite burden. Conversely, anti JAM-C treatment increased the IL-4-driven T helper 2 (Th2) response in BALB/c mice with disease exacerbation. Overall, our results show that JAM-C blockade can finely-tune the innate cell migration and accelerate the consequent immune response to L. major without changing the type of the T helper cell response