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Antigens multiple sclerosis

Andrographolide, thus, has different mechanisms of anti-inflammatory activity. It can inhibit the activation of NF-kB, suppress inducible nitric oxide synthase (iNOS) expression, inhibit COX-2 expression in human fibroblast cells and also prevent oxygen radical production by human. The compound is also able to modulate T-cell activation both in vitro as well as in vivo, it is evident that it could prevent initial T-cell priming by interfering with DC maturation and antigen presentation capacity. Therefore, andrographolide may have utility as a therapeutic agent for the treatment of autoimmune diseases, such as multiple sclerosis. " ... [Pg.343]

Polyspecific Response Associated with CNS Autoimmune Diseases. The oligoclonal, intrathecally synthesized IgG contains numerous specific antibodies and autoantibodies. Antibodies are frequently found with specificities against measles, the rubella virus and the varicella-zoster virus, but seldom against the herpes simplex virus. The occurrence of one, two, or three of these antibodies is referred to as the MRZ reaction. The corresponding antigens are not present in these cases. The MRZ reaction is typical of multiple sclerosis as well as cerebral lupus erythematosus and is a chronically evolving immune process (F5, KIO, S16). [Pg.27]

The presence of oligoclonal free kappa and lambda chains in CSF is a sensitive indication for recent antigenic immune response within the central nervous system, comparable with IgM. The detection of oligoclonal free kappa chains in CSF supports the diagnosis of multiple sclerosis. In addition, free light chains can also be found in the CSF of patients having inflammatory diseases of the central nervous system (LI). [Pg.32]

The molecular mechanism by which IFN-/1 induces its therapeutic effect is complex and not fully understood. It is believed that the pathology of multiple sclerosis is linked to the activation and proliferation of T lymphocytes specific for epitopes found on specific myelin antigens. Upon migration to the brain, these lymphocytes trigger an inflammatory response mediated by the production of pro-inflammatory cytokines, most notably IFN-y, IL-1, IL-2 and TNF-a. The inflammatory response, in addition to other elements of immunity (e.g. antibodies and... [Pg.213]

While the specific mechanisms of action of interferon-pia and interferon-pib in MS are not fully understood, each interferon has a number of immune-mediating activities (see Section 7.1). A recent review article on multiple sclerosis observed The interferons reduce the proliferation of T cells and the production of tumor necrosis factor a, decrease antigen presentation, alter cytokine production to favor ones governed by type 2 helper T (Th2) cells, increase the secretion of interleukin-10, and reduce the passage of immune cells across the blood-brain barrier by means of their effects on adhesion molecules, chemokines, and proteases [2]. [Pg.186]

HLA (human leukocyte antigen) DR2 is strongly positively correlated with SLE and multiple sclerosis, and negatively correlated with diabetes mellitus type 1. HLA DR3 is correlated strongly with Sjogren s syndrome, myasthenia gravis, SLE and diabetes mellitus type 1. HLA DR4 is correlated with the genesis of rheumatoid arthritis and diabetes mellitus type 1. [Pg.240]

Determinations of antigen by the quantitative precipitin method were used routinely for many years in some institutions for the estimation of IgG in human cerebrospinal fluid, increases in cerebrospinal fluid IgG being found in multiple sclerosis and in neurosyphilis.In recent... [Pg.20]

DeVries GH (2004) Cryptic axonal antigens and axonal loss in multiple sclerosis. Neurochem Res 29 1999-2006. [Pg.252]

Horiuchi I, Kawano Y, Yamasaki K, Minohara M, Furue M, Taniwaki T, Miyazaki T, Kira J (2000) Thl dominance in HAM/TSP and the optico-spinal form of multiple sclerosis versus Th2 dominance in mite antigen-specific IgE myelitis. J Neurol Sci 172 17-24. [Pg.323]

Bertrams J, Kuwert E, Liedtke U (1972) HL-A antigens and multiple sclerosis. Tissue Antigens 2 405 08. [Pg.473]


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See also in sourсe #XX -- [ Pg.642 ]




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