alexa Repeated Streptococcus Pyogenes Infections Induce An Autoimmune Th17 Cell Phenotype In The Brain And Impair Blood-brain Barrier Integrity: A Mouse Model For PANDAS | 61535
ISSN: 2329-6895

Journal of Neurological Disorders
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2nd International Conference on Neuroimmunology & Therapeutics
December 01-02, 2016 Atlanta, USA

Tyler Cutforth, Maryann Platt and Dritan Agalliu
Columbia University Medical Center, USA
Posters & Accepted Abstracts: J Neurol Disord
DOI: 10.4172/2329-6895.C1.015
Abstract
Streptococcus pyogenes infections are associated with two autoimmune diseases of the CNS: the movement disorder Sydenham’s chorea and the neuropsychiatric syndrome PANDAS (Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcus infections). This bacterium is known to induce autoreactive, mimetic antibodies against several CNS targets. Delivery of such antibodies in the mouse brain induces behavioral and motor deficits that are reminiscent of PANDAS symptoms, supporting their causal role in this disease. How such autoreactive antibodies cross the blood-brain barrier (BBB) to attack CNS targets, however, is unknown. We have found that intranasal S. pyogenes infections lead to an antigen-specific Th17 cell response in the nasal associated lymphoid tissue (NALT), a functional analog of human tonsils. Repeated infections drive those cells towards an IL-17+ IFN-γ+ phenotype that has been implicated in BBB breakdown during many autoimmune diseases. Moreover, repeated infections promote entry of S. Pyogenes specific T cells into the olfactory bulb and other CNS regions, whereas the bacteria remain within the nasal cavity. We also find microglial activation and barrier breakdown in close proximity to CNS-infiltrating T cells, as measured by leakage of both serum IgG and a low molecular weight tracer (biocytin-TMR), as well as disruption of endothelial cell tight junctions. These findings provide novel insight into how recurrent Streptococcus infections might impair brain function and lead to motor and neuropsychiatric diseases and suggest a general mechanism by which infectious agents that induce Th17 immunity might exacerbate other CNS autoimmune diseases such as multiple sclerosis to provoke long-term neurovascular damage.
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