Particulate antigens administrated by intranasal and intravaginal routes in a prime-boost strategy improve HIV-specific T generation, high-quality antibodies and long-lasting mucosal immunity.

Mucosal surfaces serve as the primary entry points for pathogens such as SARS- CoV-2 coronavirus or HIV in the human body. Mucosal vaccination plays a crucial role to successfully induce long-lasting systemic and local immune responses to confer sterilizing immunity. However, antigen formulations and delivery methods must be properly selected since they are decisive for the quality and the magnitude of the elicited immune responses in mucosa.

T cells lack IL-2Rα but express decoy IL-1R2 and IL-1Ra and suppress the IL-1-dependent activation of T cells.

Follicular regulatory T (T) cells from lymph node germinal centers control follicular helper T (T) cell-dependent B cell activation. These scarce cells, often described and purified as CD25 cells, are thought to be derived from thymic regulatory T (T) cells. However, we observed that mouse T cells do not respond to interleukin-2 (IL-2), unlike T cells.

TGF- and VEGF cooperatively control the immunotolerant tumor environment and the efficacy of cancer immunotherapies.

Tregs imprint an early immunotolerant tumor environment that prevents effective antitumor immune responses. Using transcriptomics of tumor tissues, we identified early upregulation of VEGF and TGF-β pathways compatible with tolerance imprinting. Silencing of VEGF or TGF-β in tumor cells induced early and pleiotropic modulation of immune-related transcriptome signatures in tumor tissues.

Low-Dose IL-2 Induces Regulatory T Cell-Mediated Control of Experimental Food Allergy.

Regulatory T cells (Tregs) are pivotal for maintenance of immune self-tolerance and also regulate immune responses to exogenous Ags, including allergens. Both decreased Treg number and function have been reported in allergic patients, offering new therapeutic perspectives. We previously demonstrated that Tregs can be selectively expanded and activated by low doses of IL-2 (ld-IL-2) inducing immunoregulation without immunosuppression and established its protective effect in autoimmune diseases.