L'attribution causale : le cas des étudiants de l'Université de Genève et des Hautes écoles suite aux résultats des évaluations sommatives

Pour Jean-Marie Vaysse (2004), l'homme est un animal évaluateur, agissant selon des fins. A l'Université, les notes sont parmi les raisons d'agir les plus importantes de l'étudiant. C'est justement l'évaluation des notes par les étudiants à travers l'attribution qui retient notre attention dans ce travail. A quoi les étudiants de l'Université de Genève et des Hautes écoles attribuent leurs échecs et leurs réussites ou tout simplement leurs notes ? En fait, l'attribution est un processus cognitif qui permet d'expliquer ce qui nous arrive (auto-attribution), ou ce qui arrive aux autres (hétéro-attribution) (Heider, 1958 ; Pansu & al., 2005 ; Sanchez-Mazas & al. 2012). C'est une psychologie de sens commun (Moscovici & Hewstone, 1984). Comme méthodologie, nous avons analysé les données qualitatives résultant de nos entretiens semi-directifs avec onze étudiants. Notre analyse a porté sur différents concepts de la psychologie sociale en lien avec l'attribution. Nos résultats ont principalement montré que les participants font les deux attributions à la fois..

Intestinal lamina propria TcRgammadelta+ lymphocytes selectively express IL-10 and IL-17

BACKGROUND: The characteristics and roles of gut lymphocytes have been only partly elucidated, in particular with regard to activation patterns. OBJECTIVES: To characterize lymphocytes from various parts of the gut and examine their activation pattern as a network. METHODS: Lymphocytes were isolated from the epithelium, the lamina propria, Peyer's patches, mesenteric lymph nodes, the spleen, and peripheral blood of naive mice. They were then characterized for T cell phenotype, T cell receptors (TcRs), activation markers, and cytokine production. RESULTS: The results showed a gradient of cells with an increasing proportion of TcRgammadelta+, CD8alphaalpha+ cells towards the gut lumen, with the highest number found in intraepithelial lymphocytes. These cells, together with lamina propria lymphocytes (LPLs) were also characterized by a memory-like phenotype (CD25- CD45RB(low) and CD44(high)) and CD69 expression. CD8+ TcRgammadelta+ LPLs produced IL-10 and IL-17, while TcRalphabeta+ LPLs were FoxP3 positive. CONCLUSIONS: Gut lymphocytes express various receptors and cytokines according to their location. These specific features suggest a differential function for gut lymphocytes depending on their location

Gut T cell receptor-gammadelta(+) intraepithelial lymphocytes are activated selectively by cholera toxin to break oral tolerance in mice

Item does not contain fulltextThe gut immune system is usually tolerant to harmless foreign antigens such as food proteins. However, tolerance breakdown may occur and lead to food allergy. To study mechanisms underlying food allergy, animal models have been developed in mice by using cholera toxin (CT) to break tolerance. In this study, we identify T cell receptor (TCR)-gammadelta(+) intraepithelial lymphocytes (IELs) as major targets of CT to break tolerance to food allergens. TCR-gammadelta(+) IEL-enriched cell populations isolated from mice fed with CT and transferred to naive mice hamper tolerization to the food allergen beta-lactoglobulin (BLG) in recipient mice which produce anti-BLG immunoglobulin (Ig)G1 antibodies. Furthermore, adoptive transfer of TCR-gammadelta(+) cells from CT-fed mice triggers the production of anti-CT IgG1 antibodies in recipient mice that were never exposed to CT, suggesting antigen-presenting cell (APC)-like functions of TCR-gammadelta(+) IELs. In contrast to TCR-alphabeta(+) cells, TCR-gammadelta(+) IELs bind and internalize CT both in vitro and in vivo. CT-activated TCR-gammadelta(+) IELs express major histocompatibility complex (MHC) class II molecules, CD80 and CD86 demonstrating an APC phenotype. CT-activated TCR-gammadelta(+) IELs migrate to the lamina propria, where they produce interleukin (IL)-10 and IL-17. These results provide in-vivo evidence for a major role of TCR-gammadelta(+) IELs in the modulation of oral tolerance in the pathogenesis of food allergy