Thèse Ciblage Spécifique des Lymphocytes t Pathogènes dans l'Auto-Immunité H/F Doctorat.Gouv.Fr
- Montpellier - 34
- CDD
- Bac +5
- Service public d'état
Les missions du poste
Les candidat(e)s disposant d'une solide formation en immunologie et manifestant un intérêt pour la recherche translationnelle sont encouragé(e)s à postuler.
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Currently, there is no cure for Type 1 diabetes and only one disease-modifying biological immunotherapy, an anti-CD3 modified monoclonal antibody, that has been recently approved. In Type 1 Diabetes, T lymphocytes target and progressively destroy the *****-producing beta cells of the pancreas. Immune destruction of beta cells involves both CD8+ and CD4+ T cells. Encounter of potentially autoreactive T cells with beta cell self-antigens occurs in the draining lymph nodes of the pancreas and is mediated by antigen presenting cells. There, in normal individuals under non-inflammatory conditions, T cells are tolerized through antigen cross-presentation and suppression by regulatory T cells. However, when the mechanisms of tolerance fail, this encounter leads to the activation of T cells. Then, activated T cells are able to migrate to the pancreas and induce beta cell destruction resulting in overt autoimmunity. Indeed, we have recently shown that beta cell-specific memory CD8+ and CD4+ T cells need to cooperate to break self-tolerance and induce autoimmunity in a transgenic mouse model. Furthermore, utilizing 2-photon microscopy, we deciphered the mechanisms via which these cell types interact in pancreas to maintain effector cell function as well as the cues that regulate their motility towards their target beta cells. (Le Saout et al. PNAS 2008 and PLoS One 2010; Espinosa et al. PLoS One 2015, Front. Immunol. 2017 et 2018). Thus, we have identified cells and pathways as target for new immunotherapeutic strategies in Type 1 diabetes (Akhter et al. Stem Cell Res Ther. 2022 and 2024).
Le profil recherché
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Publiée le 16/10/2026 - Réf : 58cfc5cff7c2b85447c84138f74c0067