Central nervous system autoimmunity

Rowse AL, Naves R, Cashman KS, McGmre DJ, Mbana T, Raman C, et al. Lithiiun controls central nervous system autoimmunity through modulation of IFN-y signaling. PLoS One 2012 7(12) e52658 (5 pages). 

McCandless EE, Budde M, Lees JR, Dorsey D, Lyng E, Klein RS (2009) IL-IR signaling within the central nervous system regulates CXCL12 expression at the blood-brain barrier and disease severity during experimental autoimmune encephalomyehtis. J Immunol 183(l) 613-620 McEarland HE, Martin R (2007) Multiple sclerosis a complicated picture of autoimmunity. Nat Immunol 8 913-919... 

Holmes EE, Arnott N, Vanderplank P et al (2008) Intra-neural administration of fractalkine attenuates neuropathic pain-related behaviour. J Neurochem 106 640-649 Huang DR, Shi ED, Jung S et al (2006) The neuronal chemokine CX3CL 1/fractalkine selectively recruits NK cells that modify experimental autoimmune encephalomyelitis within the central nervous system. EASEB J 20 896-905... 

Carpentier PA, Duncan DS, Miller SD (2008) GUal toU-hke receptor signaling in central nervous system infection and autoimmunity. Brain Behav Immun 22 140-147 Carr DJ, Serou M (1995) Exogenous and endogenous opioids as biological response modifiers. Immunopharmacology 31 59-71... 

In some instances more severe side effects are noted (Table 8.11), whereas in a few cases very serious side effects, such as induction of autoimmune reactions and central nervous system or cardiovascular disturbances, render necessary immediate withdrawal of treatment. 

Matsumoto, Y., Ohmori, K. and Fujiwara, M. Microglial and astroglial reactions to inflammatory lesions of experimental autoimmune encephalomyelitis in the rat central nervous system. /. Neuroimmunol. 37 23-33,1992. 

Khoury, S J. et al., CD28-B7 costimulatory blockade by CTLA4Ig prevents actively induced experimental autoimmune encephalomyelitis and inhibits Thl but spares Th2 cytokines in the central nervous system, J. Immunol., 155, 4521, 1995. 

La Flamme AC, Ruddenklau K, Backstrom BT Schistosomiasis decreases central nervous system inflammation and alters the progression of experimental autoimmune encephalomyelitis. Infect Immun 2003 71 4996-5004. 

McGeachy MJ, Stephens LA, Anderton SM Natural recovery and protection from autoimmune encephalomyelitis contribution ofCD4+CD25+ regulatory cells within the central nervous system. J Immunol 2005 175 3025-3032. 

Multiple sclerosis (MS) is the most frequent inflammatory demyeli-nating disease of the central nervous system that affects worldwide about 2.5 million people with no cure. Myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis (MOG-induced EAE) in DA rats is an appropriate model for therapeutic testing, sharing many features with human multiple sclerosis. 

In summary, complete examination of CSF, including basic biochemical analysis and qualitative cytology with the determination of specific CSF proteins and isoelectric focusing, provides very sensitive diagnostic imformation concerning serous inflammatory processes in the central nervous system, including diseases of autoimmune origin such as multiple sclerosis. 

Schwartz, M., Protective autoimmunity as a T-cell response to central nervous system trauma prospects for therapeutic vaccines. Prog Neurobiol, 2001. 65(5) 489-96. 

Carmody RJ, Hilliard B, Maguschak K, Chodosh LA, Chen YH. Genomic scale profiling of autoimmune inflammation in the central nervous system The nervous response to inflammation. J Neuroimmunol 2002 133(1—2) 95—107. 

In contrast to T cells, in different immunopathologies, the brain provides a fostering envkonment to B cells. Primary central nervous system (CNS) lymphomas are usually of B cell origin. The cerebrospinal fluid (CSF) of patients with chronic infections and autoimmune diseases of the CNS typically contains remarkably stable oligoclonal Ig bands. In the CNS of multiple sclerosis patients, clonally expanded B cells and plasma cells persist. Ectopic B cell follicles develop in the meninges of patients with secondary progressive MS, and B cell differentiation may be recapitulated in the CNS of MS patients (Krumbholz et al., 2006) (see Chapters 18-24). 

Moalem G, Leibowitz-Amit R, Yoles E, Mor F, Cohen IR, Schwartz M (1999) Autoimmune T cells protect neurons from secondary degeneration after central nervous system axotomy. Nat Med 5 49-55. 

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