Session 3
Neuroimmune interactions: challenges for hazard identification
Programme of the Session
- S03-01
Early life neuroinflammation as a key process setting the stage for later cognitive outcomes
Natalia Marchetti, Laura Gerosa, Fabrizio Gardoni, Jennifer Stanic, Corrado Galli, Marina Marinovich, Barbara Viviani
Department of Pharmacological and Biomolecular Sciences, University of Milan, Milan, Italy - S03-02
Brain innate immunity kindled by dopaminergic toxicants
Frederico Pereira1,2, Sofia Viana1,2,3, Carlos Fontes Ribeiro1,2
1Institute of Pharmacology and Experimental Therapeutics/IBILI, Faculty of Medicine, University of Coimbra, Coimbra, Portugal; 2CNC.IBILI, Univ. of Coimbra, Coimbra, Portugal; 3Department of Pharmacy, Polytechnic Institute of Coimbra, ESTESC-Coimbra Health School, Coimbra, Portugal
- S03-03
Combining in vitro neurotoxicity data and toxicokinetic modelling: a case study of glycol ethers
Jenny Sandström1,2, Marie-Gabrielle Zurich2,1, Florianne Tschudi-Monnet2,1, Elena Reale3
1Swiss Centre for Applied Human Toxicology, Basel, Switzerland; 2Department of Physiology, University of Lausanne, Lausanne, Switzerland; 3Institut ramand de Santé au Travail (IST), Epalinges / Lausanne, Switzerland
Session Abstract
In the last decades, substantial progress has been made in the understanding of neuroimmune interactions. Interactions between the central nervous system (CNS) and the immune system occur and are not limited to pathology but also extend to homeostatic functions. It has been demonstrated that the immune response in the CNS has both beneficial and detrimental effects on brain function; CNS-derived antigens induce an immune response in the cervical lymph nodes; and the CNS possesses a functional lymphatic system. Chemical-induced changes in immune responses, particularly within the CNS, are now thought to play a critical role in neurodisorders. Alterations in lymphocyte activity and number, changes in cytokine signaling, impairments in phagocytic functions, and glial activation and gliosis have all been reported and suggested to be implicated in neurological diseases.
This symposium aims to discussing these findings and their implication for hazard identification and mechanistic understanding.
In the last decades, substantial progress has been made in the understanding of neuroimmune interactions. Interactions between the central nervous system (CNS) and the immune system occur and are not limited to pathology but also extend to homeostatic functions. It has been demonstrated that the immune response in the CNS has both beneficial and detrimental effects on brain function; CNS-derived antigens induce an immune response in the cervical lymph nodes; and the CNS possesses a functional lymphatic system. Chemical-induced changes in immune responses, particularly within the CNS, are now thought to play a critical role in neurodisorders. Alterations in lymphocyte activity and number, changes in cytokine signaling, impairments in phagocytic functions, and glial activation and gliosis have all been reported and suggested to be implicated in neurological diseases.
This symposium aims to discussing these findings and their implication for hazard identification and mechanistic understanding.
This symposium aims to discussing these findings and their implication for hazard identification and mechanistic understanding.
In the last decades, substantial progress has been made in the understanding of neuroimmune interactions. Interactions between the central nervous system (CNS) and the immune system occur and are not limited to pathology but also extend to homeostatic functions. It has been demonstrated that the immune response in the CNS has both beneficial and detrimental effects on brain function; CNS-derived antigens induce an immune response in the cervical lymph nodes; and the CNS possesses a functional lymphatic system. Chemical-induced changes in immune responses, particularly within the CNS, are now thought to play a critical role in neurodisorders. Alterations in lymphocyte activity and number, changes in cytokine signaling, impairments in phagocytic functions, and glial activation and gliosis have all been reported and suggested to be implicated in neurological diseases.
This symposium aims to discussing these findings and their implication for hazard identification and mechanistic understanding.
