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This paper describes the conditions under which autoimmune T cells enter the central nervous system to attack the local tissue. During a prodromal period preceding the onset of neurological disease, the CNS tissue is converted from its physiological immune-hostile state to an immune-friendly state. At the same time, in the peripheral immune system, activated autoimmune T cells undergo profound changes that allow them to enter through the blood-brain barrier and to finally interact with local autoantigen-presenting cells. Antigen recognition leads to T cell activation and the secretion of inflammatory mediators that are responsible for the development of the inflammatory lesions and the neurological deficits.

Endocrine disruption is commonly thought to be restricted to a direct endocrine mode of action i.e. the perturbation of the activation of a given type of hormonal receptor by its natural ligand. Consistent with the WHO definition of an endocrine disrupter, a key issue is the “altered function(s) of the endocrine system”. Such altered functions can result from different chemical interactions, beyond agonistic or antagonistic effect at a given receptor. Based on neuroendocrine disruption by polychlorinated biphenyls and bisphenol A, this paper proposes different mechanistic paradigms that can result in adverse health effects. They are a consequence of altered endocrine function(s) secondary to chemical interaction with different steps in the physiological regulatory processes, thus accounting for a possibly indirect endocrine mode of action. [ABSTRACT FROM AUTHOR]

Abstract: This paper describes the conditions under which autoimmune T cells enter the central nervous system to attack the local tissue. During a prodromal period preceding the onset of neurological disease, the CNS tissue is converted from its physiological immune-hostile state to an immune-friendly state. At the same time, in the peripheral immune system, activated autoimmune T cells undergo profound changes that allow them to enter through the blood-brain barrier and to finally interact with local autoantigen-presenting cells. Antigen recognition leads to T cell activation and the secretion of inflammatory mediators that are responsible for the development of the inflammatory lesions and the neurological deficits. To cite this article: H. Wekerle, C. R. Biologies 330 (2007). [Copyright &y& Elsevier]