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C. L. Langrish, Y. Chen, W. M. Blumenschein, J. Mattson, B. Basham, J. D. Sedgwick, T. McClanahan, R. A. Kastelein and D. J. Cua, “IL-23 Drives a Pathogenic T Cell Population That Induces Autoimmune Inflammation,” The Journal of Experimental Medicine, Vol. 201, No. 2, 2005, pp. 233-240. doi:10.1084/jem.20041257

has been cited by the following article:

• TITLE: Initiation and Regulation of CNS Autoimmunity: Balancing Immune Surveillance and Inflammation in the CNS

  AUTHORS: Melissa G. Harris, Zsuzsanna Fabry

  KEYWORDS: CNS; Immune Surveillance, Autoimmunity; APCs; DCs; Oligodendrocyte Death; DAMPs; Initiation; Regulation

  JOURNAL NAME: Neuroscience and Medicine, Vol.3 No.3, September 25, 2012

  ABSTRACT: While the central nervous system (CNS) was once thought to be immune privileged, more recent data support that certain areas of the healthy CNS are routinely patrolled by immune cells. Further, antigen drainage is another means by which the adaptive arm of the immune system can gain information about the health of the CNS. Altogether these ensure that the CNS is not beyond the scope of immune protection against viruses and tumors. However, immune surveillance in the CNS has to be tightly regulated, as CNS autoimmune disease and inflammation may arise from increased immune cell infiltration. In this review we discuss the concept and implications of CNS immune surveillance and introduce the CNS antigen-presenting cells (APCs) that potentially regulate neuroinflammation and autoimmunity. We also discuss novel animal models in which CNS disease initiation and the role of APCs in disease regulation can be tested.