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Experimental autoimmune encephalomyelitis

In addition to antibodies targeting the CD3 subunit of the TCR complex, antibodies against the a and (3 subunits of the TCR have been tested as therapeutic agents. A benefit for the treatment experimental autoimmune encephalomyelitis or collagen induced arthritis could be shown in animal models [8]. [Pg.1180]

Lavasani S, Dzhambazov B, Andersson M (2007) Monoclonal antibody against T-cell receptor alphabeta induces self-tolerance in chronic experimental autoimmune encephalomyelitis. Scand J Immunol 65 39-47... [Pg.1181]

COPD, chronic obstructive pulmonary disease EAE, experimental autoimmune encephalomyelitis RSV, respiratory syncytial virus SLE, systemic lupus erythematosus. [Pg.1211]

Abromson-Leeman S, Bronson R, Luo Y, Berman M, Leeman R, Leeman J, Dorf M (2004) T-ceU properties determine disease site, clinical presentation, and cellular pathology of experimental autoimmune encephalomyelitis. Am J Pathol 165 1519-1533 Adamson DC, Wildemann B, Sasaki M, Glass JD, McArthur JC, Christov VI, Dawson TM, Dawson VL (1996) Immunologic NO synthase elevation in severe AIDS dementia and induction by HIV-1 gp41. Science 274 1917-1921... [Pg.136]

Glabinski AR, Bielecki B, O Bryant S, Selmaj K, Ransohoff RM (2002) Experimental autoimmune encephalomyelitis CC chemokine receptor expression by trafficking cells. J Autoimmun 19 175-181... [Pg.139]

McCandless EE, Wang Q, Woerner BM, Harper JM, Klein RS (2006) CXCL12 Umits inflammation by localizing mononuclear infiltrates to the perivascular space during experimental autoimmune encephalomyelitis. J Immunol 177 8053-8064 McCandless EE, Piccio L, Woerner BM, Schmidt RE, Rubin JB, Cross AH, Klein RS (2008a) Pathologic expression of CXCL12 at the blood brain barrier correlates with severity of multiple sclerosis. Am J Pathol... [Pg.141]

Smith SS, Bamum SR (2008) Differential expression of beta 2-integrins and cytokine production between gammadelta and alphabeta T cells in experimental autoimmune encephalomyelitis. J Leukoc Biol 83 71-79... [Pg.144]

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... [Pg.314]

Liu L, Graham G, Hu T, et al. The silent chemokine receptor D6 is required for generating T cell responses that mediate experimental autoimmune encephalomyelitis. J Immunol 2006 177(1) 17-21. [Pg.364]

Xu W, Fazekas G, Hara H, et al. Mechanism of natural killer (NK) cell regulatory role in experimental autoimmune encephalomyelitis. J Neuroimmunol 2005 163 24-30. [Pg.368]

Jahng AW, Maricic I, Pedersen B, et al. Activation of natural killer T cells potentiates or prevents experimental autoimmune encephalomyelitis. J Exp Med 2001 194 1789-1799. [Pg.368]

Heppner FL, Greter M, Marino D, et al. Experimental autoimmune encephalomyelitis repressed by microglial paralysis. Nat Med 2005 11 146-152. [Pg.368]

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. [Pg.19]

Some aspects of multiple sclerosis are reflected in the animal model experimental autoimmune encephalomyelitis, which is induced by immunization of susceptible animals with appropriate encephalogenic proteins or peptides. In these animals, if cultured adult stem cell neurospheres are injected into the bloodstream, injected cells can find their way to damaged portions of the nervous system and improve function in mice. How the injected cells augmented the recovery process is unclear. One possibility is that cells recruited to the lesions differentiated into oligodendrocytes and generated new myelin sheaths, but this seems unlikely in the face of ongoing cellular destruction. [Pg.512]

Iglesias, A., Bauer, J., Litzenburger, T. etal. T- and B-cell responses to myelin oligodendrocyte glycoprotein in experimental autoimmune encephalomyelitis and multiple sclerosis. Glia 36 220-234,2001. [Pg.651]

Lassmann, H. Experimental autoimmune encephalomyelitis. In R. A. Lazzarini (ed.), Myelin Biology and Disorders. San Diego, CA Elsevier Academic Press, 2004, pp. 1039-1071. [Pg.651]

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. [Pg.138]

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. [Pg.122]

Sewell D, Qing Z, Reinke E, et al Immunomodulation of experimental autoimmune encephalomyelitis by helminth ova immunization. Int Immunol 2003 15 59-69. [Pg.122]

CS = Contact sensitivity EAE = experimental autoimmune encephalomyelitis nt = not tested. ... [Pg.140]

Pal E, Tabira T Autonomic regulation of experimental autoimmune encephalomyelitis the role of inter-feron-y. Neuroimmunomodulation 2002 10 80-84. [Pg.148]

Jiang H, Curran S, Ruiz-Vazquez E, Liang B, Winchester R, Chess L Regulatory CDS + T cells fine-tune the myelin basic protein-reactive T cell receptor V(5 repertoire during experimental autoimmune encephalomyelitis. Proc Natl Acad Sci USA 2003 100 8378-8383. [Pg.148]


See other pages where Experimental autoimmune encephalomyelitis is mentioned: [Pg.353]    [Pg.468]    [Pg.122]    [Pg.137]    [Pg.138]    [Pg.140]    [Pg.140]    [Pg.141]    [Pg.141]    [Pg.143]    [Pg.144]    [Pg.145]    [Pg.204]    [Pg.246]    [Pg.268]    [Pg.353]    [Pg.357]    [Pg.196]    [Pg.444]    [Pg.446]    [Pg.359]    [Pg.366]    [Pg.213]    [Pg.248]    [Pg.385]    [Pg.139]   
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